pioglitazone has been researched along with Cerebral Ischemia in 39 studies
Pioglitazone: A thiazolidinedione and PPAR GAMMA agonist that is used in the treatment of TYPE 2 DIABETES MELLITUS.
pioglitazone : A member of the class of thiazolidenediones that is 1,3-thiazolidine-2,4-dione substituted by a benzyl group at position 5 which in turn is substituted by a 2-(5-ethylpyridin-2-yl)ethoxy group at position 4 of the phenyl ring. It exhibits hypoglycemic activity.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Pioglitazone improves glycaemic control, not only by lowering insulin resistance, but also by improving beta cell function." | 9.41 | In praise of pioglitazone: An economically efficacious therapy for type 2 diabetes and other manifestations of the metabolic syndrome. ( Bell, DSH; Jerkins, T, 2023) |
| " The identification of insulin resistance as a risk factor for stroke and myocardial infarction raised the possibility that pioglitazone, which improves insulin sensitivity, might benefit patients with cerebrovascular disease." | 9.22 | Pioglitazone after Ischemic Stroke or Transient Ischemic Attack. ( Adams, HP; Berger, L; Brass, LM; Carolei, A; Clark, W; Conwit, R; Coull, B; Ford, GA; Furie, KL; Gorman, M; Guarino, PD; Inzucchi, SE; Kernan, WN; Kleindorfer, D; Lovejoy, AM; O'Leary, JR; Parsons, MW; Peduzzi, PN; Ringleb, P; Schwartz, GG; Sen, S; Spence, JD; Tanne, D; Viscoli, CM; Wang, D; Winder, TR; Young, LH, 2016) |
| "While this study was too underpowered to determine the effect of pioglitazone, the result failed to show beneficial effects in patients of ischemic stroke or TIA with impaired glucose tolerance and newly diagnosed diabetes." | 9.20 | Effects of Pioglitazone for Secondary Stroke Prevention in Patients with Impaired Glucose Tolerance and Newly Diagnosed Diabetes: The J-SPIRIT Study. ( Furukawa, Y; Hattori, N; Kawamori, R; Miyamoto, N; Nakahara, T; Nakamura, S; Okuma, Y; Shimura, H; Tanaka, R; Tanaka, Y; Tomizawa, Y; Ueno, Y; Urabe, T; Watada, H; Yamashiro, K, 2015) |
| "The aim of this study was to determine the effectiveness of pioglitazone compared with placebo for improving insulin sensitivity among nondiabetic patients with a recent transient ischemic attack (TIA) or nondisabling ischemic stroke and impaired insulin sensitivity." | 9.10 | Pioglitazone improves insulin sensitivity among nondiabetic patients with a recent transient ischemic attack or ischemic stroke. ( Brass, LM; Bravata, DM; Horwitz, RI; Inzucchi, SE; Kernan, WN; McVeety, JC; Shulman, GI; Viscoli, CM, 2003) |
| "Luteolin, a flavonoid compound with anti-inflammatory activity, has been reported to alleviate cerebral ischemia/reperfusion (I/R) injury." | 8.12 | Luteolin alleviates inflammation and autophagy of hippocampus induced by cerebral ischemia/reperfusion by activating PPAR gamma in rats. ( Fan, R; Guo, L; Li, D; Li, L; Liang, H; Ma, L; Pan, G; Qiu, J, 2022) |
| "Studies assessing the efficacy of pioglitazone solely for primary stroke prevention in Asian patients with type 2 diabetes mellitus (DM) and present multiple cardiovascular (CV) risk factors are rare." | 7.96 | Pioglitazone for primary stroke prevention in Asian patients with type 2 diabetes and cardiovascular risk factors: a retrospective study. ( Bau, DT; Chiu, LT; Huang, HY; Hung, YC, 2020) |
| "In this nested case-control study using real-world data, treatment with pioglitazone exhibited significant cardiovascular preventive effect in diabetic patients with acute ischemic stroke." | 7.91 | Effect of pioglitazone in acute ischemic stroke patients with diabetes mellitus: a nested case-control study. ( Kim, J; Lee, HS; Woo, MH, 2019) |
| "In the present study, we investigated the effects of pioglitazone (PGZ) in the hippocampal CA1 region of low- or high-fat diet (LFD or HFD) fed gerbils after transient forebrain ischemia." | 7.81 | Differential Effects of Pioglitazone in the Hippocampal CA1 Region Following Transient Forebrain Ischemia in Low- and High-Fat Diet-Fed Gerbils. ( Chang, IB; Cho, BM; Cho, SM; Choi, GM; Hwang, IK; Jung, HY; Kim, DW; Moon, SM; Won, MH; Yim, HS; Yoo, DY, 2015) |
| "Present study was carried out to investigate the possible neuroprotective effect of pioglitazone, an antidiabetic agent, peroxisome proliferator-activated receptor gamma (PPARgamma) agonist on acute phase changes in mice model of cerebral ischemia induced by Bilateral Common Carotid artery Occlusion (BCCAO)." | 7.76 | Neuroprotective effect of pioglitazone on acute phase changes induced by partial global cerebral ischemia in mice. ( Aggarwal, R; Chakrabarti, A; Medhi, B, 2010) |
| "In rats subjected to cerebral ischemia, post-ischemic treatment with either dose of pioglitazone alleviated particular motor deficits and sensory impairments on day 2 after MCAO." | 6.77 | Treatment of rats with pioglitazone in the reperfusion phase of focal cerebral ischemia: a preclinical stroke trial. ( Culman, J; Glatz, T; Gohlke, P; Herdegen, T; Nguyen-Ngoc, M; Zhao, Y, 2012) |
| "Pioglitazone was also associated with reduced recurrent IS in patients who also used telmisartan (p for interaction = 0." | 5.56 | Pioglitazone and PPAR-γ modulating treatment in hypertensive and type 2 diabetic patients after ischemic stroke: a national cohort study. ( Lee, TH; Li, YR; Lin, YS; Liu, CH; Sung, PS; Wei, YC, 2020) |
| "Pioglitazone (10mg/kg; po) was administered daily for 2 weeks prior to I/R." | 5.42 | Neuroprotective effects of pioglitazone against transient cerebral ischemic reperfusion injury in diabetic rats: Modulation of antioxidant, anti-inflammatory, and anti-apoptotic biomarkers. ( Ain-Shoka, AA; Attia, AS; El-Sahar, AE; Safar, MM; Zaki, HF, 2015) |
| "Pioglitazone improves glycaemic control, not only by lowering insulin resistance, but also by improving beta cell function." | 5.41 | In praise of pioglitazone: An economically efficacious therapy for type 2 diabetes and other manifestations of the metabolic syndrome. ( Bell, DSH; Jerkins, T, 2023) |
| "Pioglitazone pretreatment also attenuated the oxidative stress and DNA fragmentation after cerebral IR injury." | 5.35 | Protective effects of pioglitazone against global cerebral ischemic-reperfusion injury in gerbils. ( Iyer, S; Kaundal, RK; Kumar, A; Sharma, SS, 2009) |
| " The identification of insulin resistance as a risk factor for stroke and myocardial infarction raised the possibility that pioglitazone, which improves insulin sensitivity, might benefit patients with cerebrovascular disease." | 5.22 | Pioglitazone after Ischemic Stroke or Transient Ischemic Attack. ( Adams, HP; Berger, L; Brass, LM; Carolei, A; Clark, W; Conwit, R; Coull, B; Ford, GA; Furie, KL; Gorman, M; Guarino, PD; Inzucchi, SE; Kernan, WN; Kleindorfer, D; Lovejoy, AM; O'Leary, JR; Parsons, MW; Peduzzi, PN; Ringleb, P; Schwartz, GG; Sen, S; Spence, JD; Tanne, D; Viscoli, CM; Wang, D; Winder, TR; Young, LH, 2016) |
| "While this study was too underpowered to determine the effect of pioglitazone, the result failed to show beneficial effects in patients of ischemic stroke or TIA with impaired glucose tolerance and newly diagnosed diabetes." | 5.20 | Effects of Pioglitazone for Secondary Stroke Prevention in Patients with Impaired Glucose Tolerance and Newly Diagnosed Diabetes: The J-SPIRIT Study. ( Furukawa, Y; Hattori, N; Kawamori, R; Miyamoto, N; Nakahara, T; Nakamura, S; Okuma, Y; Shimura, H; Tanaka, R; Tanaka, Y; Tomizawa, Y; Ueno, Y; Urabe, T; Watada, H; Yamashiro, K, 2015) |
| "The aim of this study was to determine the effectiveness of pioglitazone compared with placebo for improving insulin sensitivity among nondiabetic patients with a recent transient ischemic attack (TIA) or nondisabling ischemic stroke and impaired insulin sensitivity." | 5.10 | Pioglitazone improves insulin sensitivity among nondiabetic patients with a recent transient ischemic attack or ischemic stroke. ( Brass, LM; Bravata, DM; Horwitz, RI; Inzucchi, SE; Kernan, WN; McVeety, JC; Shulman, GI; Viscoli, CM, 2003) |
| " Pioglitazone (an oral hypoglycemic agent of the thiazolidinedione drug class) was shown in the IRIS trial to reduce the risk of recurrent stroke in patients with impaired glucose tolerance who had not developed type 2 diabetes mellitus." | 4.98 | Updates in Stroke Treatment. ( Mac Grory, B; Yaghi, S, 2018) |
| " Together with the recent observation that the PPAR-gamma ligand pioglitazone reduces the incidence of stroke in patients with type 2 diabetes, this review supports the concept that activators of PPAR-gamma are effective drugs against ischemic injury." | 4.84 | PPAR-gamma: therapeutic target for ischemic stroke. ( Culman, J; Gohlke, P; Herdegen, T; Zhao, Y, 2007) |
| "Luteolin, a flavonoid compound with anti-inflammatory activity, has been reported to alleviate cerebral ischemia/reperfusion (I/R) injury." | 4.12 | Luteolin alleviates inflammation and autophagy of hippocampus induced by cerebral ischemia/reperfusion by activating PPAR gamma in rats. ( Fan, R; Guo, L; Li, D; Li, L; Liang, H; Ma, L; Pan, G; Qiu, J, 2022) |
| "Studies assessing the efficacy of pioglitazone solely for primary stroke prevention in Asian patients with type 2 diabetes mellitus (DM) and present multiple cardiovascular (CV) risk factors are rare." | 3.96 | Pioglitazone for primary stroke prevention in Asian patients with type 2 diabetes and cardiovascular risk factors: a retrospective study. ( Bau, DT; Chiu, LT; Huang, HY; Hung, YC, 2020) |
| "In this nested case-control study using real-world data, treatment with pioglitazone exhibited significant cardiovascular preventive effect in diabetic patients with acute ischemic stroke." | 3.91 | Effect of pioglitazone in acute ischemic stroke patients with diabetes mellitus: a nested case-control study. ( Kim, J; Lee, HS; Woo, MH, 2019) |
| "In the present study, we investigated the effects of pioglitazone (PGZ) in the hippocampal CA1 region of low- or high-fat diet (LFD or HFD) fed gerbils after transient forebrain ischemia." | 3.81 | Differential Effects of Pioglitazone in the Hippocampal CA1 Region Following Transient Forebrain Ischemia in Low- and High-Fat Diet-Fed Gerbils. ( Chang, IB; Cho, BM; Cho, SM; Choi, GM; Hwang, IK; Jung, HY; Kim, DW; Moon, SM; Won, MH; Yim, HS; Yoo, DY, 2015) |
| "The role of the phosphorylated signal transducer and activator of transcription-3 (p-STAT3) after cerebral ischemia by the peroxisome proliferator-activated receptor γ (PPARγ) agonist pioglitazone (PGZ) remains controversial." | 3.78 | Activation of signal transducer and activator of transcription-3 by a peroxisome proliferator-activated receptor gamma agonist contributes to neuroprotection in the peri-infarct region after ischemia in oophorectomized rats. ( Kageji, T; Kinouchi, T; Kitazato, KT; Matsushita, N; Nagahiro, S; Satomi, J; Shimada, K; Sumiyoshi, M; Tada, Y; Yagi, K, 2012) |
| "Present study was carried out to investigate the possible neuroprotective effect of pioglitazone, an antidiabetic agent, peroxisome proliferator-activated receptor gamma (PPARgamma) agonist on acute phase changes in mice model of cerebral ischemia induced by Bilateral Common Carotid artery Occlusion (BCCAO)." | 3.76 | Neuroprotective effect of pioglitazone on acute phase changes induced by partial global cerebral ischemia in mice. ( Aggarwal, R; Chakrabarti, A; Medhi, B, 2010) |
| "In rats subjected to cerebral ischemia, post-ischemic treatment with either dose of pioglitazone alleviated particular motor deficits and sensory impairments on day 2 after MCAO." | 2.77 | Treatment of rats with pioglitazone in the reperfusion phase of focal cerebral ischemia: a preclinical stroke trial. ( Culman, J; Glatz, T; Gohlke, P; Herdegen, T; Nguyen-Ngoc, M; Zhao, Y, 2012) |
| "These mice received a middle cerebral artery occlusion and reperfusion injury, and they were evaluated for the infarct volume and by immunohistochemistry and western blotting analysis at several time points after ischemia." | 1.62 | Pioglitazone Prevents Hemorrhagic Infarction After Transient Focal Ischemia in Type 2 Diabetes. ( Arai, H; Hasegawa, H; Hattori, N; Mitome-Mishima, Y; Miyamoto, N; Oishi, H; Tanaka, R; Urabe, T; Yatomi, K, 2021) |
| "Pre-treatment with fenofibrate and pioglitazone in addition to their combination improved neurobehavioral dysfunction, reduced cerebral infarct volume, attenuated inflammatory and apoptotic markers and ameliorated histopathological changes in I/R injured rats." | 1.56 | The impact of single and combined PPAR-α and PPAR-γ activation on the neurological outcomes following cerebral ischemia reperfusion. ( Abdelrehim, AB; Ahmed, AF; Heeba, GH; Shehata, AHF, 2020) |
| "Pioglitazone was also associated with reduced recurrent IS in patients who also used telmisartan (p for interaction = 0." | 1.56 | Pioglitazone and PPAR-γ modulating treatment in hypertensive and type 2 diabetic patients after ischemic stroke: a national cohort study. ( Lee, TH; Li, YR; Lin, YS; Liu, CH; Sung, PS; Wei, YC, 2020) |
| "Pioglitazone (10mg/kg; po) was administered daily for 2 weeks prior to I/R." | 1.42 | Neuroprotective effects of pioglitazone against transient cerebral ischemic reperfusion injury in diabetic rats: Modulation of antioxidant, anti-inflammatory, and anti-apoptotic biomarkers. ( Ain-Shoka, AA; Attia, AS; El-Sahar, AE; Safar, MM; Zaki, HF, 2015) |
| "Pioglitazone or vehicle was infused intracerebroventricularly over a 5-day period before, during and 24 or 48 h after middle cerebral artery occlusion." | 1.36 | Peroxisome-proliferator-activated receptors gamma and peroxisome-proliferator-activated receptors beta/delta and the regulation of interleukin 1 receptor antagonist expression by pioglitazone in ischaemic brain. ( Culman, J; Glatz, T; Gohlke, P; Herdegen, T; Nguyen-Ngoc, M; Stöck, I; Zhao, Y, 2010) |
| " Translation of these findings into clinical therapy will require careful assessment of dosing paradigms and effective time windows for treatment." | 1.36 | Extension of the neuroprotective time window for thiazolidinediones in ischemic stroke is dependent on time of reperfusion. ( Blankenship, DA; Gamboa, J; Hilow, E; Karl, M; Landreth, GE; Niemi, JP; Sundararajan, S, 2010) |
| "Pioglitazone treatment reduced the infarct size and improved neurological functions." | 1.35 | Peroxisome proliferator-activated receptorsgamma (PPARgamma) differently modulate the interleukin-6 expression in the peri-infarct cortical tissue in the acute and delayed phases of cerebral ischaemia. ( Culman, J; Gohlke, P; Herdegen, T; Patzer, A; Stöck, I; Zhao, Y, 2008) |
| "Pioglitazone pretreatment also attenuated the oxidative stress and DNA fragmentation after cerebral IR injury." | 1.35 | Protective effects of pioglitazone against global cerebral ischemic-reperfusion injury in gerbils. ( Iyer, S; Kaundal, RK; Kumar, A; Sharma, SS, 2009) |
| "Pioglitazone or vehicle were i." | 1.33 | The intracerebral application of the PPARgamma-ligand pioglitazone confers neuroprotection against focal ischaemia in the rat brain. ( Culman, J; Gohlke, P; Herdegen, T; Patzer, A; Zhao, Y, 2005) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 9 (23.08) | 29.6817 |
| 2010's | 22 (56.41) | 24.3611 |
| 2020's | 8 (20.51) | 2.80 |
| Authors | Studies |
|---|---|
| Li, L | 1 |
| Pan, G | 1 |
| Fan, R | 1 |
| Li, D | 1 |
| Guo, L | 1 |
| Ma, L | 1 |
| Liang, H | 1 |
| Qiu, J | 1 |
| Guo, Y | 1 |
| Zuo, W | 1 |
| Yin, L | 1 |
| Gu, T | 1 |
| Wang, S | 1 |
| Fang, Z | 1 |
| Wang, B | 1 |
| Dong, H | 1 |
| Hou, W | 1 |
| Zuo, Z | 1 |
| Deng, J | 1 |
| Bell, DSH | 1 |
| Jerkins, T | 1 |
| Liu, CH | 1 |
| Lee, TH | 1 |
| Lin, YS | 1 |
| Sung, PS | 1 |
| Wei, YC | 1 |
| Li, YR | 1 |
| Shehata, AHF | 1 |
| Ahmed, AF | 1 |
| Abdelrehim, AB | 1 |
| Heeba, GH | 1 |
| Hung, YC | 1 |
| Chiu, LT | 1 |
| Huang, HY | 1 |
| Bau, DT | 1 |
| Hasegawa, H | 1 |
| Yatomi, K | 1 |
| Mitome-Mishima, Y | 1 |
| Miyamoto, N | 2 |
| Tanaka, R | 2 |
| Oishi, H | 1 |
| Arai, H | 1 |
| Hattori, N | 2 |
| Urabe, T | 2 |
| Zhao, Y | 7 |
| Lützen, U | 1 |
| Gohlke, P | 7 |
| Jiang, P | 1 |
| Herdegen, T | 7 |
| Culman, J | 7 |
| Katsiki, N | 1 |
| Mikhailidis, DP | 1 |
| Rydén, L | 1 |
| Mellbin, L | 1 |
| Hankey, GJ | 1 |
| Musso, G | 1 |
| Cassader, M | 1 |
| Gambino, R | 1 |
| Jin-Shan, H | 1 |
| Xue-Bin, L | 1 |
| Young, LH | 2 |
| Viscoli, CM | 3 |
| Inzucchi, SE | 3 |
| Kernan, WN | 3 |
| Mac Grory, B | 1 |
| Yaghi, S | 1 |
| Dawson, J | 1 |
| Woo, MH | 1 |
| Lee, HS | 1 |
| Kim, J | 1 |
| Duelsner, A | 1 |
| Gatzke, N | 1 |
| Hillmeister, P | 1 |
| Glaser, J | 1 |
| Zietzer, A | 1 |
| Nagorka, S | 1 |
| Janke, D | 1 |
| Pfitzner, J | 1 |
| Stawowy, P | 1 |
| Meyborg, H | 1 |
| Urban, D | 1 |
| Bondke Persson, A | 1 |
| Buschmann, IR | 1 |
| Moon, SM | 1 |
| Choi, GM | 1 |
| Yoo, DY | 1 |
| Jung, HY | 1 |
| Yim, HS | 1 |
| Kim, DW | 1 |
| Hwang, IK | 1 |
| Cho, BM | 1 |
| Chang, IB | 1 |
| Cho, SM | 1 |
| Won, MH | 1 |
| Yu, SJ | 1 |
| Reiner, D | 1 |
| Shen, H | 1 |
| Wu, KJ | 1 |
| Liu, QR | 1 |
| Wang, Y | 1 |
| Yamashiro, K | 1 |
| Okuma, Y | 1 |
| Shimura, H | 1 |
| Nakamura, S | 1 |
| Ueno, Y | 1 |
| Tanaka, Y | 1 |
| Tomizawa, Y | 1 |
| Nakahara, T | 1 |
| Furukawa, Y | 1 |
| Watada, H | 1 |
| Kawamori, R | 1 |
| El-Sahar, AE | 1 |
| Safar, MM | 1 |
| Zaki, HF | 1 |
| Attia, AS | 1 |
| Ain-Shoka, AA | 1 |
| Macan, M | 1 |
| Vukšić, A | 1 |
| Žunec, S | 1 |
| Konjevoda, P | 1 |
| Lovrić, J | 1 |
| Kelava, M | 1 |
| Štambuk, N | 1 |
| Vrkić, N | 1 |
| Bradamante, V | 1 |
| Furie, KL | 1 |
| Gorman, M | 1 |
| Guarino, PD | 1 |
| Lovejoy, AM | 1 |
| Peduzzi, PN | 1 |
| Conwit, R | 1 |
| Brass, LM | 2 |
| Schwartz, GG | 1 |
| Adams, HP | 1 |
| Berger, L | 1 |
| Carolei, A | 1 |
| Clark, W | 1 |
| Coull, B | 1 |
| Ford, GA | 1 |
| Kleindorfer, D | 1 |
| O'Leary, JR | 1 |
| Parsons, MW | 1 |
| Ringleb, P | 1 |
| Sen, S | 1 |
| Spence, JD | 1 |
| Tanne, D | 1 |
| Wang, D | 1 |
| Winder, TR | 1 |
| Patzer, A | 3 |
| Stöck, I | 2 |
| Lee, SR | 1 |
| Kim, HY | 1 |
| Hong, JS | 1 |
| Baek, WK | 1 |
| Park, JW | 1 |
| Kaundal, RK | 1 |
| Iyer, S | 1 |
| Kumar, A | 1 |
| Sharma, SS | 1 |
| Glatz, T | 2 |
| Nguyen-Ngoc, M | 2 |
| Gamboa, J | 1 |
| Blankenship, DA | 1 |
| Niemi, JP | 1 |
| Landreth, GE | 1 |
| Karl, M | 2 |
| Hilow, E | 2 |
| Sundararajan, S | 2 |
| Medhi, B | 1 |
| Aggarwal, R | 1 |
| Chakrabarti, A | 1 |
| Blankenship, D | 1 |
| Niemi, J | 1 |
| Kinouchi, T | 1 |
| Kitazato, KT | 1 |
| Shimada, K | 1 |
| Yagi, K | 1 |
| Tada, Y | 1 |
| Matsushita, N | 1 |
| Sumiyoshi, M | 1 |
| Satomi, J | 1 |
| Kageji, T | 1 |
| Nagahiro, S | 1 |
| Bravata, DM | 1 |
| Shulman, GI | 1 |
| McVeety, JC | 1 |
| Horwitz, RI | 1 |
| Shimazu, T | 1 |
| Inoue, I | 1 |
| Araki, N | 1 |
| Asano, Y | 1 |
| Sawada, M | 1 |
| Furuya, D | 1 |
| Nagoya, H | 1 |
| Greenberg, JH | 1 |
| Collino, M | 1 |
| Aragno, M | 1 |
| Mastrocola, R | 1 |
| Gallicchio, M | 1 |
| Rosa, AC | 1 |
| Dianzani, C | 1 |
| Danni, O | 1 |
| Thiemermann, C | 1 |
| Fantozzi, R | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Preventive Effects of Ginseng Against Atherosclerosis and Subsequent Ischemic Stroke: A Randomized Controlled Trial[NCT02796664] | 58 participants (Actual) | Interventional | 2016-06-23 | Completed | |||
| Insulin Resistance Intervention After Stroke (IRIS) Trial[NCT00091949] | Phase 3 | 3,876 participants (Actual) | Interventional | 2005-02-28 | Completed | ||
| The Effect of Liraglutide Treatment on Postprandial Chylomicron and VLDL Kinetics, Liver Fat and de Novo Lipogenesis - a Single-center Randomized Controlled Study[NCT02765399] | Phase 4 | 23 participants (Actual) | Interventional | 2015-02-01 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
We calculated average drug compliance based on the number of remained drugs at each follow-up. (NCT02796664)
Timeframe: At twelve months after randomization.
| Intervention | percentage of drug compliance (Mean) |
|---|---|
| Ginseng | 97.4 |
| Placebo | 97.8 |
Presence of other cerebro-cardiovascular morbidity or mortality assessed by aggravation of patient status (modified Rankin Scale). The modified Rankin Scale is ranging from 0 to 5. The higher scale indicates the worse outcome. (NCT02796664)
Timeframe: Twelve months after randomization.
| Intervention | Participants (Count of Participants) | |||||
|---|---|---|---|---|---|---|
| mRS 0 | mRS 1 | mRS 2 | mRS 3 | mRS 4 | mRS 5 | |
| Ginseng | 21 | 5 | 0 | 2 | 0 | 0 |
| Placebo | 22 | 1 | 0 | 1 | 0 | 0 |
The 1-year composite of cerebral ischemic stroke and transient ischemic attack downstream to an atherosclerotic lesion (NCT02796664)
Timeframe: Twelve months after randomization.
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| Ischemic stroke | Transient ischemic attack | |
| Ginseng | 0 | 0 |
| Placebo | 0 | 1 |
The changes in volumetric blood flow (ml/sec) in intracranial vessels assessed by quantitative magnetic resonance angiography with noninvasive optimal vessel analysis. (NCT02796664)
Timeframe: At randomization and twelve months after randomization.
| Intervention | Participants (Count of Participants) | |||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| The flow change in steno-occlusive lesion72501839 | The flow change in steno-occlusive lesion72501838 | The flow change in collateral vessel72501838 | The flow change in collateral vessel72501839 | |||||||||
| Improved | No change | Aggravated | ||||||||||
| Ginseng | 4 | |||||||||||
| Placebo | 5 | |||||||||||
| Ginseng | 17 | |||||||||||
| Placebo | 18 | |||||||||||
| Placebo | 1 | |||||||||||
| Ginseng | 7 | |||||||||||
| Placebo | 7 | |||||||||||
| Placebo | 9 | |||||||||||
| Placebo | 8 | |||||||||||
The changes of white matter hyperintensities, assessed by the Fazekas scale using brain magnetic resonance imaging. The Fazekas scale is a 4 point white matter disease severity scale with values ranging from 0 to 3. It quantifies the amount of white matter T2 hyperintense lesions each in periventricular white matter and deep white matter. Higher scales mean a worse white matter status. In the region of the periventricular white matter, 0 means absence of the lesion; 1, caps or pencil-thin lining lesion; 2, smooth halo lesion; 3, irregular high intense signal extending into the deep shite matter. In the region of the deep white matter, 0 means absence of the lesion; 1, punctate foci lesions; 2, beginning confluence; 3, large confluent hyperintense areas. (NCT02796664)
Timeframe: At randomization and twelve months after randomization.
| Intervention | Participants (Count of Participants) | |||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Periventricular white matter72501836 | Periventricular white matter72501837 | Deep white matter72501837 | Deep white matter72501836 | |||||||||||||
| Fazekas scale 3 | Fazekas scale 0 | Fazekas scale 1 | Fazekas scale 2 | |||||||||||||
| Placebo | 11 | |||||||||||||||
| Placebo | 10 | |||||||||||||||
| Ginseng | 2 | |||||||||||||||
| Ginseng | 9 | |||||||||||||||
| Placebo | 6 | |||||||||||||||
| Ginseng | 15 | |||||||||||||||
| Placebo | 15 | |||||||||||||||
| Ginseng | 3 | |||||||||||||||
| Placebo | 2 | |||||||||||||||
| Ginseng | 1 | |||||||||||||||
| Placebo | 1 | |||||||||||||||
Fatal or non-fatal acute myocardial infarction or unstable angina (NCT00091949)
Timeframe: 5 years
| Intervention | participants (Number) |
|---|---|
| Pioglitazone | 206 |
| Placebo | 249 |
(NCT00091949)
Timeframe: 5 years
| Intervention | participants (Number) |
|---|---|
| Pioglitazone | 136 |
| Placebo | 146 |
(NCT00091949)
Timeframe: 5 years
| Intervention | participants (Number) |
|---|---|
| Pioglitazone | 206 |
| Placebo | 249 |
Change in modified mental status examination (3MS) score from baseline to exit. Theoretical range of 3MS scores is 0-100. Baseline scores ranged from 22-100. (NCT00091949)
Timeframe: Annual measures from baseline to exit (up to 5 years)
| Intervention | units on a scale (Mean) |
|---|---|
| Pioglitazone | 0.27 |
| Placebo | 0.29 |
(NCT00091949)
Timeframe: 5 years
| Intervention | participants (Number) |
|---|---|
| Pioglitazone | 73 |
| Placebo | 149 |
(NCT00091949)
Timeframe: 5 years
| Intervention | participants (Number) |
|---|---|
| Pioglitazone | 127 |
| Placebo | 154 |
(NCT00091949)
Timeframe: Up to 5 years
| Intervention | participants (Number) |
|---|---|
| Pioglitazone | 175 |
| Placebo | 228 |
Before vs after intervention (Liraglutide or placebo): Change in body weight. Results from Matikainen et al. Diabetes Obes Metab 21:84-94; 2019. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | kg (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 98.6 | 96.1 |
| Placebo | 92.0 | 89.8 |
Before vs after intervention (Liraglutide or placebo): apolipoprotein CIII concentration in plasma measured by using turbidimetric immunoassay. Results from Matikainen et al. Diabetes Obes Metab 21:84-94; 2019. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | mg/dL (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 12.0 | 9.9 |
| Placebo | 9.7 | 8.6 |
Before vs after intervention (Liraglutide or placebo): Direct apoB48 clearance rates in isolated chylomicrons and measured by liquid chromatography - mass spectrometry and calculated by multicompartmental modeling assay. The power of mathematical modelling to describe the metabolic pathways of lipid and lipoprotein metabolism was demonstrated by Zech L et al (1979). So far few studies have focused on the modelling of apo B48 and apo B100 after a meal that is more physiological than the fasting state (Björnson E et al. 2019). Production rates for apo B48, apo B100 and triglycerides in chylomicrons, VLDL1 and VLDL2 were derived from samples taken before and after the tracer injection and after the meal at 0, 30, 45, 60, 75, 90,120, 150 min and at 3, 4, 5, 6, 8, 10, 24 hrs and averages for 24 hrs. Analysis of tracer/ tracee curves of stable isotopes was used to derived the estimates of kinetic parameters using a new mathematical modeling per day. Results from Taskinen et al. 2021. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | mg/day (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 106 | 3.8 |
| Placebo | 20 | 17 |
Before vs after intervention (Liraglutide or placebo): concentration of fasting plasma glucose measured using the hexokinase method. Results from Matikainen et al. Diabetes Obes Metab 21:84-94; 2019. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | mmol/L (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 8.3 | 6.4 |
| Placebo | 6.5 | 6.4 |
Before vs after intervention (Liraglutide or placebo): Change in B -Hemoglobiini-A1c level in plasma. Results from Matikainen et al. Diabetes Obes Metab 21:84-94; 2019. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | HbA1c % (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 7.0 | 6.4 |
| Placebo | 6.3 | 6.4 |
Before vs after intervention (Liraglutide or placebo): Hepatic DNL is calculated from enrichment of deuterated water ingested during the kinetic study at specified time points (0, 4 and 8 hrs.). Results from Matikainen et al. Diabetes Obes Metab 21:84-94; 2019. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | μmol/L (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 15.4 | 19.1 |
| Placebo | 12.6 | 13.8 |
Before vs after intervention (Liraglutide or placebo): Concentration of insulin level in plasma measured using electrochemiluminescence. Results from Matikainen et al. Diabetes Obes Metab 21:84-94; 2019. (NCT02765399)
Timeframe: Baseline and after16 weeks
| Intervention | μU/mL (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 13.9 | 14.5 |
| Placebo | 13.8 | 14.1 |
Before vs after intervention (Liraglutide or placebo): mean liver fat content was measured by magnetic resonance imaging. Results from Matikainen et al. Diabetes Obes Metab 21:84-94; 2019. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | fat % (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 14.8 | 10.7 |
| Placebo | 16.1 | 13.9 |
Before vs after intervention (Liraglutide or placebo): Matsuda index was calculated for assessment of insulin sensitivity in plasma at time points 0, 30, 60 and 120 minutes using formula 10,000/square root of [fasting glucose x fasting insulin] x [mean glucose x mean insulin during oral glucose tolerance test]. The Matsuda index is considered to be the gold standard to determine insulin sensitivity without glucose clamp studies (Matsuda M, DeFronzo RA. Diabetes Care. 22:1462-70). Subjects who don't have insulin resistance have values of Matsuda Index of 2.5 or higher (Kerman WN et al. Stroke 34:1431;2003). Results from Matikainen et al. Diabetes Obes Metab 21:84-94; 2019. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | index (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 2.5 | 3.5 |
| Placebo | 3.1 | 3.1 |
Before vs after intervention (Liraglutide or placebo): subcutaneous adipose tissue area measured by magnetic resonance imaging (MRI). Results from Matikainen et al. Diabetes Obes Metab 21:84-94; 2019. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | cm3 (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 4043 | 3792 |
| Placebo | 5400 | 5161 |
Before vs after intervention (Liraglutide or placebo): systolic blood pressure measurements. Results from Matikainen et al. Diabetes Obes Metab 21:84-94; 2019. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | mm Hg (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 135 | 139 |
| Placebo | 145 | 137 |
Before vs after intervention (Liraglutide or placebo): visceral adipose tissue area measured by magnetic resonance imaging (MRI). Results from Matikainen et al. Diabetes Obes Metab 21:84-94; 2019. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | cm3 (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 3403 | 3185 |
| Placebo | 2710 | 2600 |
Before vs after intervention (Liraglutide or placebo): Change in apoB48 chylomicron fractional transfer rate to VLDL1 isolated from plasma by ultracentrifugation and by liquid chromatography/mass spectrometry and calculated with multicompartmental modeling assay. So far few studies have focused on the modelling of apo B48 and apo B100 after a meal that is more physiological than the fasting state (Björnson E et al. JIM 2019). Production rates for apo B48, apo B100 and triglycerides in chylomicrons, VLDL1 and VLDL2 were derived from samples taken before and after the tracer injection and after the meal at 0, 30, 45, 60, 75, 90,120, 150 min and at 3, 4, 5, 6, 8, 10, 24 hrs and averages for 24 hrs. Analysis of tracer/ tracee curves of stable isotopes was used to derived the estimates of kinetic parameters using a new mathematical modeling per day. Results from Taskinen et al. 2021. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | pools/day (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 12 | 26 |
| Placebo | 34 | 30 |
Before vs after intervention (Liraglutide or placebo): Change in chylomicron fractional direct clearance rates of apoB48 measured from plasma by liquid chromatography - mass spectrometry with multicompartmental modeling assay. The power of mathematical modelling to describe the metabolic pathways of lipid and lipoprotein metabolism was demonstrated by Zech L et al (1979). So far few studies have focused on the modelling of apo B48 and apo B100 after a meal that is more physiological than the fasting state (Björnson E et al. 2019). Production rates for apo B48, apo B100 and triglycerides in chylomicrons, VLDL1 and VLDL2 were derived from samples taken before and after the tracer injection and after the meal at 0, 30, 45, 60, 75, 90,120, 150 min and at 3, 4, 5, 6, 8, 10, 24 hrs and averages for 24 hrs. Analysis of tracer/ tracee curves of stable isotopes was used to derived the estimates of kinetic parameters using a new mathematical modeling per day. Results from Taskinen et al. 2021. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | pools/day (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 9 | 0.8 |
| Placebo | 4.4 | 3.2 |
Before vs after intervention (Liraglutide or placebo): Change in chylomicron-apoB48 transfer rates to VLDL1 isolated from plasma by ultracentrifugation and measured using multicompartmental modeling. The power of mathematical modelling to describe the metabolic pathways of lipid and lipoprotein metabolism was demonstrated by Zech L et al (1979). So far few studies have focused on the modelling of apo B48 and apo B100 after a meal that is more physiological than the fasting state (Björnson E et al. 2019). Production rates for apo B48, apo B100 and triglycerides in chylomicrons, VLDL1 and VLDL2 were derived from samples taken before and after the tracer injection and after the meal at 0, 30, 45, 60, 75, 90,120, 150 min and at 3, 4, 5, 6, 8, 10, 24 hrs and averages for 24 hrs. Analysis of tracer/ tracee curves of stable isotopes was used to derived the estimates of kinetic parameters using a new mathematical modeling per day. Results from Taskinen et al. 2021. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | mg/day (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 127 | 110 |
| Placebo | 170 | 150 |
Before vs after intervention (Liraglutide or placebo): Change in VLDL2-apoB100 fractional catabolic rates measured from isolated VLDL2 from plasma by ultracentrifugation and measured using mathematical modeling. The power of mathematical modelling to describe the metabolic pathways of lipid and lipoprotein metabolism was demonstrated by Zech L et al (JCI 1979). So far few studies have focused on the modelling of apo B48 and apo B100 after a meal that is more physiological than the fasting state (Björnson E et al. JIM 2019). Production rates for apo B48, apo B100 and triglycerides in chylomicrons, VLDL1 and VLDL2 were derived from samples taken before and after the tracer injection and after the meal at 0, 30, 45, 60, 75, 90,120, 150 min and at 3, 4, 5, 6, 8, 10, 24 hrs and averages for 24 hrs. Analysis of tracer/ tracee curves of stable isotopes was used to derived the estimates of kinetic parameters using a new mathematical modeling per day. Results from Taskinen et al. DOM 2021. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | pools/day (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 6.7 | 5.6 |
| Placebo | 4.5 | 5.1 |
Before vs after intervention (Liraglutide or placebo): Change in mean production rate of ApoB48 in chylomicrons isolated from plasma samples and measured by multicompartmental modeling assay. The power of mathematical modelling to describe the metabolic pathways of lipid and lipoprotein metabolism was demonstrated by Zech L et al (JCI 1979). So far few studies have focused on the modelling of apo B48 and apo B100 after a meal that is more physiological than the fasting state (Björnson E et al. JIM 2019). Production rates for apo B48, apo B100 and triglycerides in chylomicrons, VLDL1 and VLDL2 were derived from samples taken before and after the tracer injection and after the meal at 0, 30, 45, 60, 75, 90,120, 150 min and at 3, 4, 5, 6, 8, 10, 24 hrs and averages for 24 hrs. Analysis of tracer/ tracee curves of stable isotopes was used to derived the estimates of kinetic parameters using a new mathematical modeling per day. Results from Taskinen et al. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | mg/day (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 284 | 113 |
| Placebo | 190 | 160 |
Before vs after intervention (Liraglutide or placebo): Change in triglycerides fractional catabolic rates in isolated chylomicrons from plasma samples measured by multicompartmental modeling assay. The power of mathematical modelling to describe the metabolic pathways of lipid and lipoprotein metabolism was demonstrated by Zech L et al (JCI 1979). So far few studies have focused on the modelling of apo B48 and apo B100 after a meal that is more physiological than the fasting state (Björnson E et al. JIM 2019). Production rates for apo B48, apo B100 and triglycerides in chylomicrons, VLDL1 and VLDL2 were derived from samples taken before and after the tracer injection and after the meal at 0, 30, 45, 60, 75, 90,120, 150 min and at 3, 4, 5, 6, 8, 10, 24 hrs and averages for 24 hrs. Analysis of tracer/ tracee curves of stable isotopes was used to derived the estimates of kinetic parameters using a new mathematical modeling per day. Results from Taskinen et al. DOM 2021. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | pools/day (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 33 | 46 |
| Placebo | 64 | 59 |
Before vs after intervention (Liraglutide or placebo): ApoB48 total production in plasma measured by using multicompartmental modeling. The power of mathematical modelling to describe the metabolic pathways of lipid and lipoprotein metabolism was demonstrated by Zech L et al (JCI 63:1262;1979) and have been widely used over 30yrs. So far few studies have focused on the modelling of apo B48 and apo B100 after a meal that is more physiological than the fasting state (Björnson E et al. JIM 285:562;2019). Production rates for apo B48, apo B100 and triglycerides in chylomicrons, VLDL1 and VLDL2 were derived from samples taken before and after the tracer injection and after the meal at 0, 30, 45, 60, 75, 90,120, 150 min and at 3, 4, 5, 6, 8, 10, 24 hrs and averages for 24 hrs. Analysis of tracer/ tracee curves of stable isotopes was used to derived the estimates of kinetic parameters using a new mathematical modeling per day. Results from Taskinen et al. Diabetes Obes Metab. 23:1191; 2021. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | mg/day (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 490 | 329 |
| Placebo | 570 | 530 |
Before vs after intervention (Liraglutide or placebo): Change in VLDL1 production rates measured from isolated VLDL from plasma samples by ultracentrifugation and measured using mathematical modeling. The power of mathematical modelling to describe the metabolic pathways of lipid and lipoprotein metabolism was demonstrated by Zech L et al (JCI 1979). So far few studies have focused on the modelling of apo B48 and apo B100 after a meal that is more physiological than the fasting state (Björnson E et al. JIM 2019). Production rates for apo B48, apo B100 and triglycerides in chylomicrons, VLDL1 and VLDL2 were derived from samples taken before and after the tracer injection and after the meal at 0, 30, 45, 60, 75, 90,120, 150 min and at 3, 4, 5, 6, 8, 10, 24 hrs and averages for 24 hrs. Analysis of tracer/ tracee curves of stable isotopes was used to derived the estimates of kinetic parameters using a new mathematical modeling per day. Results from Taskinen et al. DOM 2021. (NCT02765399)
Timeframe: Baseline and after16 weeks
| Intervention | g/day (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 51 | 35 |
| Placebo | 43 | 35 |
Before vs after intervention (Liraglutide or placebo): postprandial plasma TG summary measured using the trapezoidal rule and expressed as AUC (at fasting and at 0.5, 1, 2, 3, 4, 6 and 8 hours) after oral fat tolerance test. Results from Matikainen et al. Diabetes Obes Metab 21:84-94; 2019. (NCT02765399)
Timeframe: Baseline and after 16 weeks
| Intervention | mmol/l per h (Mean) | |
|---|---|---|
| Baseline | 16 weeks | |
| Liraglutide | 22.0 | 17.1 |
| Placebo | 17.5 | 19.0 |
3 reviews available for pioglitazone and Cerebral Ischemia
| Article | Year |
|---|---|
In praise of pioglitazone: An economically efficacious therapy for type 2 diabetes and other manifestations of the metabolic syndrome.
Topics: Brain Ischemia; Diabetes Mellitus, Type 2; Female; Heart Failure; Humans; Hypoglycemic Agents; Insul | 2023 |
Updates in Stroke Treatment.
Topics: Acute Disease; Atrial Fibrillation; Brain Ischemia; Glucose Intolerance; Humans; Hypoglycemic Agents | 2018 |
PPAR-gamma: therapeutic target for ischemic stroke.
Topics: Animals; Brain Ischemia; Diabetes Mellitus, Type 2; Drug Administration Routes; Drug Delivery System | 2007 |
4 trials available for pioglitazone and Cerebral Ischemia
| Article | Year |
|---|---|
Effects of Pioglitazone for Secondary Stroke Prevention in Patients with Impaired Glucose Tolerance and Newly Diagnosed Diabetes: The J-SPIRIT Study.
Topics: Adult; Aged; Aged, 80 and over; Brain Ischemia; Diabetes Mellitus, Type 2; Female; Glucose Intoleran | 2015 |
Pioglitazone after Ischemic Stroke or Transient Ischemic Attack.
Topics: Aged; Brain Ischemia; Double-Blind Method; Female; Fractures, Bone; Humans; Hypoglycemic Agents; Ins | 2016 |
Pioglitazone after Ischemic Stroke or Transient Ischemic Attack.
Topics: Aged; Brain Ischemia; Double-Blind Method; Female; Fractures, Bone; Humans; Hypoglycemic Agents; Ins | 2016 |
Pioglitazone after Ischemic Stroke or Transient Ischemic Attack.
Topics: Aged; Brain Ischemia; Double-Blind Method; Female; Fractures, Bone; Humans; Hypoglycemic Agents; Ins | 2016 |
Pioglitazone after Ischemic Stroke or Transient Ischemic Attack.
Topics: Aged; Brain Ischemia; Double-Blind Method; Female; Fractures, Bone; Humans; Hypoglycemic Agents; Ins | 2016 |
Treatment of rats with pioglitazone in the reperfusion phase of focal cerebral ischemia: a preclinical stroke trial.
Topics: Analysis of Variance; Animals; Brain Infarction; Brain Ischemia; Caspase 9; Cerebral Cortex; Cycloox | 2012 |
Pioglitazone improves insulin sensitivity among nondiabetic patients with a recent transient ischemic attack or ischemic stroke.
Topics: Aged; Blood Glucose; Brain Ischemia; Female; Glucose Tolerance Test; Humans; Hypoglycemic Agents; In | 2003 |
32 other studies available for pioglitazone and Cerebral Ischemia
| Article | Year |
|---|---|
Luteolin alleviates inflammation and autophagy of hippocampus induced by cerebral ischemia/reperfusion by activating PPAR gamma in rats.
Topics: Animals; Autophagy; Brain Ischemia; Hippocampus; Inflammation; Luteolin; Molecular Docking Simulatio | 2022 |
Pioglitazone attenuates ischaemic stroke aggravation by blocking PPARγ reduction and inhibiting chronic inflammation in diabetic mice.
Topics: Animals; Brain Ischemia; Diabetes Mellitus, Experimental; Inflammation; Ischemic Stroke; Mice; NLR F | 2022 |
Pioglitazone and PPAR-γ modulating treatment in hypertensive and type 2 diabetic patients after ischemic stroke: a national cohort study.
Topics: Aged; Antihypertensive Agents; Brain Ischemia; Databases, Factual; Diabetes Mellitus, Type 2; Female | 2020 |
The impact of single and combined PPAR-α and PPAR-γ activation on the neurological outcomes following cerebral ischemia reperfusion.
Topics: Animals; Apoptosis; Brain; Brain Ischemia; Cerebral Infarction; Disease Models, Animal; Drug Therapy | 2020 |
Pioglitazone for primary stroke prevention in Asian patients with type 2 diabetes and cardiovascular risk factors: a retrospective study.
Topics: Aged; Asian People; Brain Ischemia; Databases, Factual; Diabetes Mellitus, Type 2; Female; Humans; H | 2020 |
Pioglitazone Prevents Hemorrhagic Infarction After Transient Focal Ischemia in Type 2 Diabetes.
Topics: Adiponectin; Animals; Brain Ischemia; Diabetes Mellitus, Type 2; Humans; Infarction, Middle Cerebral | 2021 |
Neuroprotective and antioxidative effects of pioglitazone in brain tissue adjacent to the ischemic core are mediated by PI3K/Akt and Nrf2/ARE pathways.
Topics: Animals; Antioxidants; Apoptosis; Biomarkers; Brain Ischemia; Cerebrovascular Circulation; Disease M | 2021 |
Pioglitazone in patients with insulin resistance after ischemic stroke or transient ischemic attack: A comment on the IRIS trial.
Topics: Brain Ischemia; Humans; Insulin Resistance; Ischemic Attack, Transient; Pioglitazone; Stroke | 2017 |
New Hope For People With Dysglycemia and Cardiovascular Disease Manifestations: Reduction of Acute Coronary Events With Pioglitazone.
Topics: Brain Ischemia; Cardiovascular Diseases; Diabetes Mellitus; Humans; Insulin Resistance; Ischemic Att | 2017 |
Which Patients With Ischemic Stroke and Insulin Resistance May Benefit From Pioglitazone Hydrochloride?
Topics: Brain Ischemia; Humans; Insulin Resistance; Ischemic Attack, Transient; Myocardial Infarction; Piogl | 2017 |
Letter by Musso et al Regarding Article, "Cardiac Outcomes After Ischemic Stroke or Transient Ischemic Attack: Effects of Pioglitazone in Patients With Insulin Resistance Without Diabetes Mellitus".
Topics: Brain Ischemia; Diabetes Mellitus; Humans; Insulin Resistance; Ischemic Attack, Transient; Pioglitaz | 2017 |
Letter by Jin-Shan and Xue-Bin Regarding Article, "Cardiac Outcomes After Ischemic Stroke or Transient Ischemic Attack: Effects of Pioglitazone in Patients With Insulin Resistance Without Diabetes Mellitus".
Topics: Brain Ischemia; Diabetes Mellitus; Humans; Insulin Resistance; Ischemic Attack, Transient; Pioglitaz | 2017 |
Response by Young et al to Letters Regarding Article, "Cardiac Outcomes After Ischemic Stroke or Transient Ischemic Attack: Effects of Pioglitazone in Patients With Insulin Resistance Without Diabetes Mellitus".
Topics: Brain Ischemia; Diabetes Mellitus; Humans; Insulin Resistance; Ischemic Attack, Transient; Pioglitaz | 2017 |
Pioglitazone Use After Stroke: Story of Hearts, Minds, and Bones.
Topics: Brain Ischemia; Heart Failure; Humans; Hypoglycemic Agents; Insulin; Ischemic Attack, Transient; Pio | 2018 |
Effect of pioglitazone in acute ischemic stroke patients with diabetes mellitus: a nested case-control study.
Topics: Aged; Brain Ischemia; Databases, Factual; Diabetes Mellitus, Type 2; Female; Humans; Hypoglycemic Ag | 2019 |
PPARγ activation inhibits cerebral arteriogenesis in the hypoperfused rat brain.
Topics: Angiogenesis Inducing Agents; Animals; Blotting, Western; Brain; Brain Ischemia; Disease Models, Ani | 2014 |
Differential Effects of Pioglitazone in the Hippocampal CA1 Region Following Transient Forebrain Ischemia in Low- and High-Fat Diet-Fed Gerbils.
Topics: Animals; Brain Ischemia; CA1 Region, Hippocampal; Cell Death; Diet, Fat-Restricted; Diet, High-Fat; | 2015 |
Time-Dependent Protection of CB2 Receptor Agonist in Stroke.
Topics: Animals; Behavior, Animal; Brain Ischemia; Calcium-Binding Proteins; Cannabinoid Receptor Agonists; | 2015 |
Neuroprotective effects of pioglitazone against transient cerebral ischemic reperfusion injury in diabetic rats: Modulation of antioxidant, anti-inflammatory, and anti-apoptotic biomarkers.
Topics: Animals; Antioxidants; Apoptosis; Apoptosis Regulatory Proteins; Brain Ischemia; Carotid Artery, Com | 2015 |
Effects of simvastatin on malondialdehyde level and esterase activity in plasma and tissue of normolipidemic rats.
Topics: Animals; Antioxidants; Apoptosis; Apoptosis Regulatory Proteins; Brain Ischemia; Carotid Artery, Com | 2015 |
Peroxisome proliferator-activated receptorsgamma (PPARgamma) differently modulate the interleukin-6 expression in the peri-infarct cortical tissue in the acute and delayed phases of cerebral ischaemia.
Topics: Animals; Anti-Inflammatory Agents; Brain Ischemia; Cerebral Infarction; Disease Models, Animal; Ence | 2008 |
PPARgamma agonist pioglitazone reduces matrix metalloproteinase-9 activity and neuronal damage after focal cerebral ischemia.
Topics: Animals; Brain Ischemia; Cerebral Infarction; Cytoprotection; Male; Matrix Metalloproteinase Inhibit | 2009 |
Protective effects of pioglitazone against global cerebral ischemic-reperfusion injury in gerbils.
Topics: Animals; Brain Ischemia; Disease Models, Animal; DNA Fragmentation; Gerbillinae; Hippocampus; Hyperk | 2009 |
Peroxisome-proliferator-activated receptors gamma and peroxisome-proliferator-activated receptors beta/delta and the regulation of interleukin 1 receptor antagonist expression by pioglitazone in ischaemic brain.
Topics: Animals; Brain; Brain Ischemia; Cerebral Infarction; Infarction, Middle Cerebral Artery; Interleukin | 2010 |
Extension of the neuroprotective time window for thiazolidinediones in ischemic stroke is dependent on time of reperfusion.
Topics: Animals; Behavior, Animal; Blood Pressure; Brain; Brain Ischemia; Cell Adhesion Molecules; Disease M | 2010 |
Neuroprotective effect of pioglitazone on acute phase changes induced by partial global cerebral ischemia in mice.
Topics: Acute-Phase Reaction; Animals; Antioxidants; Brain Edema; Brain Ischemia; Carotid Artery, Common; Ce | 2010 |
Oral pioglitazone reduces infarction volume and improves neurologic function following MCAO in rats.
Topics: Administration, Oral; Animals; Brain Ischemia; Cerebral Infarction; Disease Models, Animal; Hypoglyc | 2011 |
Activation of signal transducer and activator of transcription-3 by a peroxisome proliferator-activated receptor gamma agonist contributes to neuroprotection in the peri-infarct region after ischemia in oophorectomized rats.
Topics: Animals; Apoptosis; Basal Ganglia; Brain; Brain Ischemia; Caspase 3; Cell Nucleus; Cerebral Infarcti | 2012 |
A peroxisome proliferator-activated receptor-gamma agonist reduces infarct size in transient but not in permanent ischemia.
Topics: Animals; Blood-Brain Barrier; Blotting, Western; Brain; Brain Ischemia; Cerebrovascular Circulation; | 2005 |
The intracerebral application of the PPARgamma-ligand pioglitazone confers neuroprotection against focal ischaemia in the rat brain.
Topics: Animals; Brain; Brain Edema; Brain Ischemia; Cerebral Infarction; Disease Models, Animal; Encephalit | 2005 |
Modulation of the oxidative stress and inflammatory response by PPAR-gamma agonists in the hippocampus of rats exposed to cerebral ischemia/reperfusion.
Topics: Animals; Brain Ischemia; Cyclooxygenase 2; Hippocampus; Inflammation; Injections, Intravenous; Lipid | 2006 |
Activation of cerebral peroxisome proliferator-activated receptors gamma promotes neuroprotection by attenuation of neuronal cyclooxygenase-2 overexpression after focal cerebral ischemia in rats.
Topics: Animals; Brain Ischemia; Cell Survival; Cerebral Cortex; Cerebrovascular Circulation; Cyclooxygenase | 2006 |