oleuropein has been researched along with Reperfusion-Injury* in 8 studies
1 review(s) available for oleuropein and Reperfusion-Injury
1 trial(s) available for oleuropein and Reperfusion-Injury
7 other study(ies) available for oleuropein and Reperfusion-Injury
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Oleuropein ameliorated lung ischemia-reperfusion injury by inhibiting TLR4 signaling cascade in alveolar macrophages.
Lung ischemia-reperfusion (I/R) injury is a common postoperative complication in patients with lung transplantation, pulmonary embolism, and cardiopulmonary bypass. Lung I/R injury is a sterile inflammatory process that leads to lung dysfunction, and is an important cause of patient death. Effectively alleviating lung I/R injury can thus improve the prognosis of patients. In this study, we created a mouse model of lung I/R injury by transient unilateral left pulmonary artery occlusion. 6-8 weeks male C57BL/6 mice were randomly assigned to four groups: Sham, I/R, I/R + oleuropein (OLE) and OLE. OLE (50 mg/kg) was orally 24 h and 30 min before anesthesia. Measurement of lung pathohistological, isolated alveolar macrophages (AMs), inflammatory mediators, TLR4 and its downstream factors (MyD88, NF-κB) were performed. We then evaluated the ability of oleuropein (OLE) to ameliorate I/R-induced lung injury and explored the possible molecular mechanisms. OLE ameliorated I/R-induced lung injury and edema and decreased inflammatory factors in lung tissue and bronchoalveolar lavage fluid. This protection required toll-like receptor 4 (TLR4). OLE significantly inhibited I/R-induced expression of TLR4 and its downstream factors in lung tissue and alveolar macrophages. In addition, hypoxia-inducible factor 1α protein accumulated in TLR4-mediated lung I/R injury, and further induced the production of inflammatory factors. Collectively, these data suggest that OLE ameliorates I/R-induced lung injury. The mechanism responsible for its protective effect may involve inhibition of the I/R-induced inflammatory response by downregulating the TLR4 signaling cascade in AMs. Topics: Animals; Iridoid Glucosides; Lung; Lung Injury; Macrophages, Alveolar; Male; Mice; Mice, Inbred C57BL; NF-kappa B; Reperfusion Injury; Toll-Like Receptor 4 | 2022 |
Oleuropein attenuates testicular ischemia-reperfusion by inhibiting apoptosis and inflammation.
Ischemia-reperfusion injury (IRI) is the key reason of injury after testicular torsion and may eventually lead to male infertility. Oleuropein, a natural antioxidant isolated from Olea europaea, has shown beneficial effects in different models of ischemia. We evaluated the effects of oleuropein on testicular IRI and explored the underlying protective mechanisms.. A mouse testicular torsion/detorsion (T/D) model and an oxygen-glucose deprivation/reperfusion (OGD/R) germ cell model were established and treated with oleuropein. H&E staining was used to evaluate testicular pathological changes. Apoptosis and apoptosis-associated protein levels in testis tissues were assessed by TUNEL staining, immunohistochemical staining and western blot. Apoptosis levels and apoptosis-associated protein levels in GC-1 were evaluated by flow cytometry, immunofluorescence and western blot. Oxidative stress levels were assessed by malondialdehyde (MDA) and superoxide dismutase (SOD) kits. Cell viability and inflammatory protein levels were evaluated by CCK-8 assay coupled with qRT-PCR.. Relative to the control group, SOD activity was markedly suppressed, while MDA, Bax, Caspase-3, TNF-α as well as IL-1β levels were significantly increased in the T/D model and OGD/R model. However, all of the aforementioned alterations were relieved by oleuropein treatment.. Our findings indicate that oleuropein may be a promising treatment option to attenuate testicular IRI via its anti-oxidant, anti-inflammatory as well as anti-apoptotic properties. Topics: Animals; Antioxidants; Apoptosis; bcl-2-Associated X Protein; Caspase 3; Glucose; Humans; Inflammation; Iridoid Glucosides; Ischemia; Male; Malondialdehyde; Mice; Oxidative Stress; Oxygen; Reperfusion; Reperfusion Injury; Spermatic Cord Torsion; Superoxide Dismutase; Testis; Tumor Necrosis Factor-alpha | 2022 |
Effect of oleuropein on oxidative stress, inflammation and apoptosis induced by ischemia-reperfusion injury in rat kidney.
This study aimed to evaluate the effect of oleuropein (OLE), the main phenolic compound present in olive leaves, on kidney ischemia-reperfusion injury (IRI) and to explore the underlying protective mechanism.. Rat kidneys were subjected to 60 min of bilateral warm ischemia followed by 120 min of reperfusion. OLE was administered orally 48 h, 24 h and 30 min prior to ischemia at doses of 10, 50 and 100 mg/kg body weight. The creatinine, urea, uric acid concentrations and lactate dehydrogenase (LDH) activity in plasma were evaluated. Oxidative stress and inflammation parameters were also assessed. Renal expression of AMP-activated protein kinase (p-AMPK), endothelial nitric oxide synthase (eNOS), mitogen-activated protein kinases (MAPK), inflammatory proteins and apoptotic proteins were evaluated using Western blot.. Our results showed that OLE at 50 mg/kg reduced kidney IRI as revealed by a significant decrease of plasmatic creatinine, urea, uric acid concentrations and LDH activity. In parallel, OLE up-regulated antioxidant capacities. Moreover, OLE diminished the level of CRP and the expression of cyclooxygenase 2 (COX-2). Finally, OLE enhanced AMPK phosphorylation as well as eNOS expression whereas MAPK, and cleaved caspase-3 implicated in cellular apoptosis were attenuated in the ischemic kidneys.. In conclusion, this study shows that OLE could be used as therapeutic agent to reduce IRI through its anti-oxidative, anti-inflammatory and anti-apoptotic properties. Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Apoptosis; Dose-Response Relationship, Drug; Inflammation; Iridoid Glucosides; Iridoids; Kidney; Male; Oxidative Stress; Rats; Rats, Wistar; Reperfusion Injury; Time Factors | 2020 |
Protective Effects of Oleuropein Against Cerebral Ischemia/Reperfusion by Inhibiting Neuronal Apoptosis.
BACKGROUND In this study, we investigated the potential neuroprotective effect of oleuropein (OLE) on apoptotic changes via modulating Akt/glycogen synthase kinase 3 beta (Akt/GSK-3b) signaling in a rat model of cerebral ischemia/reperfusion injury (IRI). MATERIAL AND METHODS Sprague-Dawley male rats (12 weeks, n=200) were randomly assigned to 5 groups: sham group, vehicle (IRI+ vehicle) group, OLE (IRI+OLE) group, OLE+LY294002 (IRI+OLE+LY294002) group, and LY294002(IRI+LY294002) group. The rats were subjected to cerebral ischemia/reperfusion injury (IRI) model and treated once daily for 5 days with vehicle and OLE (100 mg/kg via intraperitoneal injection) after IRI injury. LY294002 (0.3 mg/kg) was intraperitoneally injected once at 30 min after IRI injury. Brain edema, neurological deficit, rotarod latencies, and Morris water maze (MWM) performance were evaluated after IRI. The number of dead cells were assayed by TUNEL staining. Western blot was used to detect the expression of Bcl-2, Bax, cleaved caspase-3 (CC3), neurotrophic factors, and the phosphorylation levels of Akt and GSK-3β. RESULTS Compared with the vehicle group, brain water content, neurological deficits, rotarod latencies, and escape latency following IRI were reduced in the OLE group. Cell apoptosis and reduced neurotrophic factor caused by IRI was also attenuated by OLE. Furthermore, increased p-Akt and decreased p-GSK-3β were caused by OLE, which were associated with decrease of Bax/Bcl-2 ratio and the suppression of Caspase-3 activity after IRI. Importantly, all the beneficial effects of OLE in the vehicle group were abrogated by PI3K inhibitor LY294002. CONCLUSIONS Cerebral ischemia was protected by OLE via suppressing apoptosis through the Akt/GSK-3β pathway and upregulating neurotrophic factor after IRI. Topics: Animals; Apoptosis; Brain; Brain Ischemia; Disease Models, Animal; Glycogen Synthase Kinase 3 beta; Infarction, Middle Cerebral Artery; Iridoid Glucosides; Iridoids; Male; Neurons; Neuroprotective Agents; Oncogene Protein v-akt; Phosphatidylinositol 3-Kinases; Phosphorylation; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Signal Transduction | 2018 |
Oleuropein, a natural extract from plants, offers neuroprotection in focal cerebral ischemia/reperfusion injury in mice.
Oleuropein (OLE) was found to have anti-inflammatory and anti-oxidant effects. The latest study has shown that it can resist myocardial injury that follows an acute myocardial infarction and can rescue impaired spinal nerve cells. In this study, we investigated the neuroprotective effects of OLE on cerebral ischemia and reperfusion injury in a middle cerebral artery occlusion model in mice.OLE (100 mg/kg) was injected intraperitoneally 1h before ischemia. We found that the volume of cerebral infarction was significantly reduced after 75 min of ischemia and 24 h of reperfusion compared with the I/R (ischemia/reperfusion) group. This protective function occurred in a dose-dependent manner. We also found that treatment with OLE could reduce the cerebral infarct volume. The neuroprotective effect was prolonged from 2 h to 4 h when we injected OLE intracerebroventricularly after reperfusion. We then found that OLE can decrease the level of cleavedcaspase-3, an important marker of apoptosis, in the ischemic mouse brain. Finally, we explored the role of OLE in providing anti-apoptotic effects through the increased expression of Bcl-2 and the decreased expression of Bax, which are important markers in apoptosis. As shown above, the function and safety of OLE in cardiovascular disease may indicate that it is a potential therapeutic for stroke. Topics: Animals; Apoptosis; bcl-2-Associated X Protein; Brain; Caspase 3; Infarction, Middle Cerebral Artery; Iridoid Glucosides; Iridoids; Male; Mice, Inbred ICR; Neurons; Neuroprotection; Neuroprotective Agents; Olea; Plant Extracts; Plant Leaves; Proto-Oncogene Proteins c-bcl-2; Reperfusion Injury | 2016 |
Effects of oleuropein and pinoresinol on microvascular damage induced by hypoperfusion and reperfusion in rat pial circulation.
The present study was aimed to assess the in vivo acute effects of oleuropein or/and pinoresinol, polyphenols widely diffused in natural sources, on rat pial microvascular responses during transient BCCAO and reperfusion.. Rat pial microcirculation was visualized by fluorescence microscopy through a closed cranial window. Pial arterioles were classified into five orders of branching. Capillaries were assigned order 0, the smallest arterioles order 1 and the largest ones order 5.. Rats subjected to BCCAO and reperfusion showed: arteriolar diameter decrease, microvascular leakage, leukocyte adhesion in venules, and reduction in capillary perfusion. Pretreatment with oleuropein or pinoresinol, a higher dose before BCCAO determined dilation in all arteriolar orders RE. Microvascular leakage was reduced as well as leukocyte adhesion and ROS formation, while capillary perfusion was protected. Inhibition of endothelium nitric oxide synthase prior to oleuropein or pinoresinol reduced the effect of these polyphenols on pial arteriolar diameter and leakage. These substances, administered together, prevented microvascular damage to a larger extent.. Oleuropein and pinoresinol were both able to protect pial microcirculation from I-reperfusion injury, to increase nitric oxide release and to reduce oxidative stress preserving pial blood flow distribution. Topics: Animals; Arterioles; Brain Injuries; Cerebrovascular Circulation; Furans; Iridoid Glucosides; Iridoids; Lignans; Male; Microcirculation; Rats; Rats, Wistar; Reperfusion Injury; Vasodilator Agents | 2015 |
Effects of a polyphenol present in olive oil, oleuropein aglycone, in a murine model of intestinal ischemia/reperfusion injury.
Dietary olive oil supplementation and more recently, olive oil phenols have been recommended as important therapeutic interventions in preventive medicine. Ole has several pharmacological properties, including antioxidant, anti-inflammatory, antiatherogenic, anticancer, antimicrobial, and antiviral and for these reasons, is becoming an important subject of study in recent years. The aim of this study was to investigate the effects of Ole aglycone on the modulation of the secondary events in mice subjected to intestinal IRI. This was induced in mice by clamping the superior mesenteric artery and the celiac trunk for 30 min, followed by release of the clamp, allowing reperfusion for 1 h. After 60 min of reperfusion, animals were killed for histological examination of the ileum tissue and immunohistochemical localization of proinflammatory cytokines (TNF-α and IL-1β) and adhesion molecules (ICAM-1 and P-sel); moreover, by Western blot analysis, we investigated the activation of NF-κB and IκBα. In addition, we evaluated the apoptosis process, as shown by TUNEL staining and Bax/Bcl-2 expressions. The results obtained by the histological and molecular examinations showed in Ole aglycone-treated mice, a decrease of inflammation and apoptosis pathway versus SAO-shocked mice. In conclusion, we propose that the olive oil compounds, in particular, the Ole aglycone, could represent a possible treatment against secondary events of intestinal IRI. Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Apoptosis; Blotting, Western; Cell Adhesion Molecules; Cytokines; Disease Models, Animal; Immunohistochemistry; In Situ Nick-End Labeling; Intestinal Diseases; Iridoid Glucosides; Iridoids; Male; Mice; Olive Oil; Plant Oils; Polyphenols; Pyrans; Reperfusion Injury | 2013 |