hydroxysafflor-yellow-a and Inflammation

Atherosclerosis (AS), a chronic arterial disease, is one of the major causes of morbidity and mortality worldwide. Several treatment modalities have been demonstrated to be effective in treating AS; however, the mortality rate due to AS remains high. Sonodynamic therapy (SDT) is a promising new treatment using low-intensity ultrasound in combination with sonosensitizers. Although SDT was developed from photodynamic therapy (PDT), it has a stronger tissue-penetrating capability and exhibits a more focused effect on the target lesional site requiring treatment. Furthermore, SDT has been demonstrated to suppress the formation of atheromatous plaques, and it can increase plaque stability both in vitro and in vivo. In this article, we critically summarize the recent literature on SDT, focusing on its possible mechanism of action as well as the existing and newly discovered sonosensitizers and chemotherapeutic agents for the treatment of AS.

Topics: Animals; Anthracenes; Antineoplastic Agents; Apoptosis; Atherosclerosis; Berberine; Cell Death; Chalcone; Curcumin; Emodin; Humans; Inflammation; Macrophages; Matrix Metalloproteinases; Mice; Neoplasms; Perylene; Photochemotherapy; Plaque, Atherosclerotic; Quinones; Reactive Oxygen Species; THP-1 Cells; Ultrasonic Therapy

Macrophage-mediated inflammatory infiltration and pathological lymphangiogenesis around atherosclerotic plaques are newly highlighted treatment targets of atherosclerosis. Although the effect of Hydroxysafflor yellow A(HSYA) on atherosclerosis was clear, few studies focus on the regulation of HSYA on such mechanisms.. This study aimed to uncover the key site of HSYA on improving atherosclerosis by regulating macrophage-induced inflammation and lymphangiogenesis.. This study was designed to explore the new mechanism of HSYA on alleviating atherosclerosis in vitro and in vivo.. In vivo, HSYA reduced the plaque formation, hepatic steatosis and inflammation-related lymphangiogenesis (IAL). It also changed the serum levels of inflammation (VEGF-C, TNF-α, IL-6, VCAM1, MCP1), lipid indexes (LDL, CHOL, TRIG) and relevant lymphangiogenesis (VEGF-C and LYVE-1) and inflammation (VCAM-1 and IL-6) signals in the aorta. In vitro, HSYA regulated Akt/mTOR and NF-κB activation by the inhibition of PI3K in macrophages.. HSYA affects inflammation and inflammation-associated lymphangiogenesis via suppressing PI3K to affect AKT/mTOR and NF-B pathway activation in macrophages, showing a comprehensive protective effect on atherosclerosis.

Topics: Animals; Apolipoproteins E; Atherosclerosis; Inflammation; Interleukin-6; Lymphangiogenesis; Macrophages; Mice; Mice, Knockout, ApoE; Molecular Docking Simulation; NF-kappa B; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; TOR Serine-Threonine Kinases; Vascular Endothelial Growth Factor C

KOA characterized by recurrent joint pain and progressive joint dysfunction. Is the present clinical common chronic progressive degenerative osteoarthropathy, how long the disease is difficult to cure and easy to relapse. Exploring new therapeutic approaches and mechanisms is important for the treatment of KOA. One of the main applications for sodium hyaluronate (SH) in the medical field is treatment of osteoarthritis. However, the effects of SH alone in the treatment of KOA are limited. Hydroxysafflor yellow A (HSYA) may have therapeutic effects for KOA.. The study intended to investigate the therapeutic effects and possible mechanisms of action HSYA+SH for cartilage tissue of rabbits with KOA and to provide a theoretical basis for the treatment of KOA.. The research team performed an animal study.. The study that took place at Liaoning Jijia Biotechnology, Shenyang, Liaoning, China.. The animals were 30 healthy, adult, New Zealand white rabbits, weighing 2-3 kg.. The research team randomly divided the rabbits into three groups, with 10 rabbits in each group: (1) a control group, for which the research team didn't induce KOA and provided no treatment; (2) the HSYA+SH group, the intervention group, for which the research team induced KOA and injected the rabbits with the HSYA+SH treatment; and (3) the KOA group, for which the research team induced KOA and injected the rabbits with saline.. The research team: (1) observed the morphological changes in the cartilage tissue using hematoxylin-eosin (HE) staining; (2) measured levels of serum inflammatory factors, including tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), interferon gamma (IFN-γ), IL-6, and IL-17 using an enzyme-linked immunosorbent assay (ELISA); (3) measured cartilage-cell apoptosis using "terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling" (TUNEL); and (4) used Western Blot to detect the expression of proteins related to the "neurogenic locus notch homolog protein 1" (Notch1) signaling pathway.. Compared with the control group, morphological changes had occurred to the cartilage tissue in the KOA group. Compared with the control group, that group's level of apoptosis was higher, the levels of serum inflammatory factors were significantly higher (P < .05), and the protein expression related to the Notch1 signaling pathway was also significantly higher (P < .05). The morphology of the cartilage tissue in the HSYA+SH was better than that of the KOA group but not as good as that of the control group. Compared with the KOA group, the HSYA+SH group's level of apoptosis was lower, the levels of serum inflammatory factors were significantly lower (P < .05), and the protein expression related to the Notch1 signaling pathway was also significantly lower (P < .05).. HSYA+SH can reduce the cellular apoptosis in the cartilage tissue of rabbits with KOA, downregulate the levels of inflammatory factors, and protect against KOA-induced cartilage tissue injury, and the mechanism may be related to the regulation of the Notch1 signaling pathway.

Topics: Animals; Hyaluronic Acid; Inflammation; Osteoarthritis, Knee; Quinones; Rabbits

To investigate the therapeutic benefits of Hydroxysafflor yellow A (HSYA) on blood-brain barrier (BBB) vulnerability after traumatic brain injury (TBI) and identify its potential action of mechanisms on TBIinduced injuries.. The rat TBI model was performed by using a controlled cortical impact device. The BBB permeability induced by TBI was measured through Evans Blue dye superflux and western blotting or polymerase chain reaction (PCR) for tight junctional proteins (TJPs). The post-TBI changes in oxidative stress markers, inflammatory response and neuron apoptosis in brain tissue were also tested.. Herein, the results showed that HSYA acutely attenuated BBB permeability via increasing the production of the TJPs, including occludin, claudin-1 and zonula occludens protein 24 h after TBI. Additionally, HSYA could suppress the secretion of proinflammatory factors, such as interleukin-1β, interleukin-6, and tumor necrosis factor-α (IL-1β, IL-6, and TNF-α), and also concurrently down-regulate the expression of inflammation-related Toll-like receptor 4/nuclear factor kappa-B (TLR4/NF-kB) protein. These HSYA challenged changes were accompanied by the decreased TBI induced oxidative stress markers and inhibited the expression of apoptosis proteins Bax, caspase-3 and caspase-9.. Taken together, all findings suggested that HSYA (30 mg/kg) are against TBI through improving the integrity in BBB, which are associated with the antioxidant, anti-inflammation and antiapoptosis via the probable mechanism of down-regulation of the TLR4/NF-kB pathway, and its in-detail protective mechanisms are under study.

Topics: Animals; Apoptosis; Blood-Brain Barrier; Brain Injuries, Traumatic; Chalcone; Inflammation; Oxidative Stress; Permeability; Quinones; Rats

Hydroxysafflor yellow A (HSYA) has been shown to have neuroprotective effects in cerebral infarction. However, its underlying roles in apoptosis and inflammation in Parkinson's disease (PD) are unknown.. The present study investigates the effects and underlying mechanisms of HSYA on dopaminergic (DA) neurodegeneration, inflammation, and apoptosis.. The PD model was established by 2 μL of 6-hyroxydopamine (6-OHDA) (3 μg/μL) striatal injection in C57BL/6J mice with different doses of HSYA (2, 4, or 8 mg/kg).. Administration of HSYA significantly reduced the Apomorphine (APO)-induced rotation, decreased from 122.5 ± 15.1 (6-OHDA group) to 47.2 ± 14.3 (8 mg/kg HSYA group). HSYA partially restored a deficit in the SN and STR of PD mice brains in TH. Furthermore, western blot analysis revealed that HSYA reduced inflammatory proteins, including iNOS, COX-2 and NF-κB and attenuated the elevation of DA neuronal apoptosis observed in PD. These findings indicate that HSYA protects against 6-OHDA induced DA neurodegeneration partly by regulating the MAPK inflammatory signalling pathway and apoptosis which highlight its therapeutic potential in the treatment of PD.

Topics: Animals; Apoptosis; Chalcone; Corpus Striatum; Dopamine; Dopaminergic Neurons; Dose-Response Relationship, Drug; Inflammation; Male; Mice; Mice, Inbred C57BL; Neuroprotective Agents; Oxidopamine; Parkinsonian Disorders; Quinones; Signal Transduction

To investigate the attenuating effect of Hydroxysafflor yellow A (HSYA) on inflammatory injury in chronic obstructive pulmonary disease (COPD).. Rats were randomly assigned to 7 groups according to body weight including normal control group, HSYA blank group (76.8 mg/kg), COPD group, COPD+HSYA (30, 48, 76.8 mg/kg) groups and COPD+dexamethasone (2 mg/kg), 10 in each group. Passive cigarette smoke and intratracheal instillation of lipopolysaccharides were used to establish a COPD model in rats. Hematoxylin and eosin staining of lung tissue sections was used, real-time polymerase chain reaction (PCR) was used to assay mRNA levels of some cytokines in lung tissues, the cytokines in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunosorbent assay (ELISA), Western blot analysis was used to determine phosphorylated p38 mitogen-activated protein kinase (MAPK) levels in lung tissues, and nuclear factor-κB (NF-κB) p65 protein levels in lung tissues were detected by immunohistochemistry.. Lung alveolar septa destruction, alveolus fusion, inflammatory cell infiltration, and bronchiole exudation were observed. These pathological changes were alleviated in the COPD+HSYA group. The mRNA expression of inflammatory factors were significantly increased in lung tissues from COPD rats (all P<0.01) and were inhibited by HSYA. Levels of inflammatory cytokines in BALF of COPD rats were significantly increased (all P<0.01) which were inhibited by HSYA (all P<0.01, 48, 76.8 mg/kg). The levels of p38 MAPK phosphorylation and p65 in lung tissues of COPD rats were significantly increased (all P<0.01) and were suppressed by HSYA (all P<0.01, 48, 76.8 mg/kg).. HSYA could alleviate inflammatory cell infiltration and other pathological changes in the lungs of COPD rats. HSYA inhibited inflammatory cytokine expression, and increase phosphorylation of p38 MAPK and NF-κB p65 in the lungs of COPD rats. The protective mechanism of HSYA to inhibit COPD inflammation might be by attenuating NF-κB and p38MAPK signal transduction.

Topics: Animals; Chalcone; Cytokines; Disease Models, Animal; Inflammation; MAP Kinase Signaling System; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Pulmonary Disease, Chronic Obstructive; Quinones; Rats; Transcription Factor RelA

Topics: Animals; Apoptosis; Brain Ischemia; Chalcone; Fluorine Radioisotopes; Glutamine; Infarction, Middle Cerebral Artery; Inflammation; Male; Neuroprotective Agents; Positron-Emission Tomography; Quinones; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Signal Transduction; Up-Regulation

Hydroxysafflor yellow A (HSYA) was reported to suppress inflammation in ischaemic microglia. However, the mechanism through which HSYA inhibits inflammation caused by cerebral ischaemia and reperfusion injury remains unknown. Here, we have mimicked acute cerebral ischaemia and reperfusion injury by subjecting male Sprague-Dawley rats to transient middle cerebral artery occlusion for 90 minutes and have demonstrated that toll-like receptor 9 (TLR9) was upregulated from day 3 after reperfusion, accompanied by the persistent activation of the pro-inflammatory nuclear factor-κB (NF-κB) pathway from 6 hours to day 7. HSYA was injected intraperitoneally at a dose of 6 mg/kg per day, which activated TLR9 in microglia of ischaemic cortex at 6 hours after reperfusion and then obviously suppressed the NF-κB pathway from day 1 to day 7. Meanwhile, HSYA also activated the anti-inflammatory pathway through interferon regulatory factor 3 from day 1 to day 3. The anti-inflammatory effect of HSYA was partially reversed by TLR9-siRNA interference in primary microglia, which was stimulated by oxygen-glucose deprivation and reoxygenation treatment. The regulation of TLR9-mediated inflammation by HSYA was consistent with the recovery of neurological deficits in rats.. Therefore, our findings support that HSYA exerts anti-inflammatory effects by reprogramming the TLR9 signalling pathway during treatment of acute cerebral ischaemia and reperfusion injury.

Topics: Animals; Animals, Newborn; Brain; Brain Infarction; Brain Ischemia; Cell Hypoxia; Cells, Cultured; Chalcone; Disease Models, Animal; Dose-Response Relationship, Drug; Functional Laterality; Gene Expression Regulation; Glucose; In Situ Nick-End Labeling; Inflammation; Male; Mice; Mice, Inbred C57BL; Microscopy, Confocal; Neurologic Examination; Quinones; Random Allocation; Rats; Rats, Sprague-Dawley; Reperfusion; RNA Interference; RNA, Messenger; Signal Transduction; Time Factors; Toll-Like Receptor 9; Transfection

Lipopolysaccharide (LPS)-induced neuroinflammation triggers and accelerates the pathogenesis of Parkinson's disease (PD).

Topics: Animals; Carthamus tinctorius; Cell Survival; Cells, Cultured; Chalcone; Cytokines; Humans; Inflammation; Lipopolysaccharides; Mesencephalon; Mice, Inbred C57BL; Neurons; Nitrogen Oxides; Primary Cell Culture; Quinones; Signal Transduction; Tissue Distribution; Transcription Factor RelA

We examined the effect of hydroxysafflor yellow A (HSYA) on the inflammatory response to strike-induced acute soft tissue injury in rats. Soft tissue injury was induced in rat leg muscles using a strike hammer, followed by intraperitoneal administration of HSYA at 16, 32, or 64 mg/kg. After 24 h, the rats were anaesthetized, blood and muscle samples were taken. Plasma levels of interleukin (IL)-6, IL-1β, and tumour necrosis factor (TNF)-αwere measured by enzyme-linked immunosorbent assay. Total RNA and protein were isolated from muscle tissue to determine the mRNA levels of IL-6, IL-1β, TNF-α, vascular cell adhesion molecule (VCAM)-1, and intercellular adhesion molecule (ICAM)-1, and the protein level of phosphorylated p38 mitogen-activated protein kinase (MAPK). Nuclear factor (NF)-κB expression was determined by muscle histopathology and immunohistochemistry. HSYA attenuated pathologic changes instrike-induced soft tissue inflammation. Treatment with HSYA also alleviated strike-induced increases in TNF-α, IL-1β, IL-6, VCAM-1, and ICAM-1mRNA levels and inhibited the increased activation of NF-κB and phosphorylation of p38 MAPK in muscle tissue. These findings suggest that HSYA effectively inhibits strike-induced inflammatory signal transduction in rats.

Topics: Acute Disease; Animals; Chalcone; Cytokines; Enzyme Activation; Gene Expression Regulation; Inflammation; Intercellular Adhesion Molecule-1; Male; Muscles; p38 Mitogen-Activated Protein Kinases; Quinones; Rats, Wistar; RNA, Messenger; Soft Tissue Injuries; Transcription Factor RelA; Vascular Cell Adhesion Molecule-1

This study observed attenuating effect of hydroxysafflor yellow A (HSYA), an effective ingredient of aqueous extract of Carthamus tinctorius L, on lipopolysaccharide (LPS)-induced endothelium inflammatory injury.. Eahy926 human endothelium cell (EC) line was used; thiazolyl blue tetrazolium bromide (MTT) test was assayed to observe the viability of EC; Luciferase reporter gene assay was applied to measure nuclear factor-κB (NF-κB) p65 subunit nuclear binding activity in EC; Western blot technology was used to monitor mitogen activated protein kinase (MAPKs) and NF-κB activation. Reverse transcription polymerase chain reaction (RT-PCR) method was applied to observe intercellular cell adhesion molecule-1 (ICAM-1) and E-selectin mRNA level; EC surface ICAM-1 expression was measured with flow cytometry and leukocyte adhesion to EC was assayed with Rose Bengal spectrophotometry technology.. HSYA protected EC viability against LPS-induced injury (P <0.05). LPS-induced NF-κB p65 subunit DNA binding (P <0.01) and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor α (IκBα) phosphorylation was inhibited by HSYA. HSYA attenuated LPS triggered ICAM-1 and E-selectin mRNA levels elevation and phosphorylation of p38 MAPK or c-Jun N-terminal kinase MAPK. HSYA also inhibited LPS-induced cell surface ICAM-1 protein expression P <0.01) and leukocyte adhesion to EC (P <0.05).. HSYA is effective to protect LPS-induced high expression of endothelium adhesive molecule and inflammatory signal transduction.

Topics: Cell Adhesion; Cell Nucleus; Cell Survival; Chalcone; E-Selectin; Endothelium, Vascular; Gene Expression Regulation; Human Umbilical Vein Endothelial Cells; Humans; I-kappa B Proteins; Inflammation; Intercellular Adhesion Molecule-1; Leukocytes; Lipopolysaccharides; MAP Kinase Signaling System; NF-KappaB Inhibitor alpha; Phosphorylation; Protective Agents; Protein Binding; Quinones; RNA, Messenger

To evaluate the beneficial effects of hydroxysafflor yellow A (HSYA) on monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) in rats, and to investigate the main pathophysiological mechanism of HSYA in preventing development of MCT-induced PAH.. Four groups (control, control with HSYA treatment, MCT-exposed, and MCT-exposed with HSYA treatment) were evaluated at day 28 following MCT exposure. Haemodynamic measurements, right ventricular hypertrophy, morphometry, inflammatory cytokines and oxidant expression were assessed.. HSYA significantly reduced haemodynamic changes, right ventricular hypertrophy and morphometric changes induced by exposure to MCT. HYSA also suppressed MCT-induced inflammation and oxidative stress in rat pulmonary tissue.. Experimental MCT-induced PAH may be reduced by HSYA treatment, and the mechanism may involve suppression of inflammation and oxidative stress.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Chalcone; Deoxyguanosine; Gene Expression Regulation; Hemodynamics; Hypertension, Pulmonary; Hypertrophy, Right Ventricular; Inflammation; Male; Malondialdehyde; Monocrotaline; Oxidative Stress; Quinones; Rats, Wistar; RNA, Messenger; Superoxide Dismutase; Vascular Remodeling

Inflammation is an important contributor to the development of Alzheimer's disease (AD). Anti-inflammatory medication may offer promising treatment for AD. Hydroxy-safflor yellow A (HSYA), a chemical component of the safflower yellow pigments, has been reported to exert potent immunosuppressive effects. This study examined the anti-inflammatory effects of HSYA in Aβ₁₋₄₂-treated BV-2 microglia cells. The mRNA levels of IL-1β, IL-4, IL-10, TNF-α, COX-2 and iNOS were detected by real-time PCR. Western blotting was used to determine the protein expression of COX-2, TNF-α, iNOS, Janus Kinase 2 (JAK2), p-JAK2, signal transducers and activators of transcription 3 (STAT3) and p-STAT3. BV2-conditioned medium was used to treat SH-SY5Y cells and primary neuronal cells in indirect toxicity experiments. Cell viability and apoptosis were assessed using MTT assay and Annexin V/PI staining respectively. The results demonstrated that HSYA significantly reduced the expression of the pro-inflammatory mediators and inhibited Aβ₁₋₄₂-induced neuroinflammation. Moreover, HSYA protected primary cortical neurons and SH-SY5Y cells against microglia-mediated neurotoxicity. HSYA also enhanced the phosphorylation of JAK2/STAT3 pathway and inhibition of JAK2 by AG 490 attenuated the anti-inflammatory effects of HSYA. Overall, our findings suggested that HSYA inhibited Aβ₁₋₄₂-induced inflammation and conferred neuroprotection partially through JAK2/STAT3 pathway, indicating that HSYA could be a potential drug for the treatment of AD.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Anti-Inflammatory Agents; Apoptosis; Cell Line; Chalcone; Humans; Inflammation; Microglia; Neurons; Neuroprotective Agents; Quinones; Signal Transduction

Beta-amyloid (Aβ)-mediated inflammation plays a critical role in the initiation and progression of Alzheimer׳s disease (AD). Anti-inflammatory treatment may provide therapeutic benefits. In this study, the effect of hydroxy-safflor yellow A (HSYA) on Aβ1-42-induced inflammation in AD mice was investigated and the underlying mechanisms were explored. Aβ1-42 was injected into bilateral hippocampi of mice to induce AD models in vivo. Spatial learning and memory of mice were investigated by the Morris water maze test. Activated microglia and astrocytes were examined by immunofluorescence staining for ionized calcium-binding adapter molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP). The mRNA of inflammatory cytokines were measured using real-time PCR. NF-κB p65 translocation was analyzed by western blotting and immunostaining. IκB and phosphorylation of JAK2 and STAT3 were tested by western blotting. The results showed that HSYA ameliorated the memory deficits in Aβ1-42-induced AD mice. HSYA suppressed Aβ1-42-induced activation of microglia and astrocytes and reduced the mRNA expression of pro-inflammatory mediators. HSYA up-regulated the JAK2/STAT3 pathway and inhibits the activation of NF-κB signaling pathways. Pharmacological inhibition of STAT3 by AG490 reversed the inactivation of p65 and anti-inflammatory effects of HSYA. In conclusion, these results suggest that HSYA protects Aβ1-42-induced AD model through inhibiting inflammatory response, which may involve the JAK2/STAT3/NF-κB pathway.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Cells, Cultured; Chalcone; Inflammation; Janus Kinase 2; Male; Mice; Mice, Inbred ICR; Microglia; NF-kappa B; Peptide Fragments; Quinones; Signal Transduction; Spatial Learning; STAT3 Transcription Factor

Hydroxysafflor yellow A (HSYA) is an active ingredient obtained from the flower of Carthamus tinctorius L. The present study investigated the effects of HSYA on lipopolysaccharide (LPS)-induced inflammatory signal transduction in human alveolar epithelial A549 cells. A549 cells stimulated with LPS were incubated with three doses of HSYA (1, 4 and 16μmol/L). HSYA suppressed the expression of TLR-4, Myd88, ICAM-1, TNFα, IL-1β and IL-6 at the mRNA and protein level, and inhibited the adhesion of leukocytes to A549 cells. HSYA treatment also decreased NF-κB p65 nuclear translocation and inhibited the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK). These findings suggest that HSYA effectively inhibits LPS-induced inflammatory signal transduction in A549 cells.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Cell Adhesion; Cell Line, Tumor; Chalcone; Cytokines; Epithelial Cells; Gene Expression Regulation; Humans; Inflammation; Leukocytes; Lipopolysaccharides; Molecular Structure; Myeloid Differentiation Factor 88; Quinones; Signal Transduction; Toll-Like Receptor 4; Transcription Factor RelA

Hydroxysafflor Yellow A has been demonstrated to attenuate pressure overloaded hypertrophy in rats and inhibit platelet aggregation. Herein we found that Hydroxysafflor Yellow A prevented cerebral ischemia-reperfusion injury by inhibition of thrombin generation. In addition, treatment with Hydroxysafflor Yellow A significantly inhibited NF-kappaB p65 nuclear translation and p65 binding activity, both mRNA and protein levels of ICAM-1 and the infiltration of neutrophils. Mean while, Hydroxysafflor Yellow A had the capacity to improve neurological deficit scores, increase the number of the surviving hippocampal CA1 pyramidal cells and decrease the plasma angiotensin II level. These results illustrated that anti-cerebral ischemic mechanism of Hydroxysafflor Yellow A may be due to its suppression of thrombin generation and inhibition of thrombin-induced inflammatory responses by reducing angiotensin II content.

Topics: Animals; Brain Ischemia; Chalcone; Inflammation; Male; Quinones; Rats; Rats, Wistar; Reperfusion Injury; Thrombin

Previous data demonstrated that hydroxysafflor yellow A (HSYA), a yellow color pigments extracted from the safflower, was an effective agent against focal cerebral ischemia. In the present study we demonstrated that HSYA prevented the injury in cultured cerebral cortical neurons induced by oxygen-glucose deprivation and increased the cell viability, as shown by the inhibition of both LDH and NO efflux. Further, HSYA administered orally 3 d before middle cerebral artery occlusion has the capacity to reduce cerebral infarct size and edema after 2 h cerebral ischemia followed by 24 h reperfusion in rats, and to significantly improve neurological behavior scores. Mean while, treatment with HSYA significantly decreased both mRNA and protein levels of IL-1beta, TNF-alpha in ischemic brain tissue. These results suggested that the protection of HSYA results from, at least in part, suppression of inflammatory responses following focal ischemia reperfusion.

Topics: Animals; Behavior, Animal; Blotting, Western; Brain Edema; Cell Hypoxia; Cells, Cultured; Chalcone; Female; Glucose; Indicators and Reagents; Inflammation; Interleukin-1beta; Ischemic Attack, Transient; L-Lactate Dehydrogenase; Neurons; Neuroprotective Agents; Nitric Oxide; Pregnancy; Quinones; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Reverse Transcriptase Polymerase Chain Reaction; Tumor Necrosis Factor-alpha