Reducing the levels of ET-1 and IL-6 in ischemia-reperfusion injury rats with Hydroxyethylpuerarin
Ziying Wang
Abstract
Ziying Wang
Abstract
PurposeTo investigate the effect of hydroxyethylpuerarin on the levels of ET-1 and IL-6 in focal brain ischemia-reperfusion injury rats.MethodsRats were divided into 6 groups randomly,ie.sham-operate group,ischemia-reperfusion group,hydroxyethylpuerarin 15 mg/kg,30 mg/kg,60 mg/kg groups and nimodipine 0.2 mg/kg group.Rats were prepared with a model of focal brain ischemic injury by middle cerebral artery occlusion(MCAO),then recovered perfusion by pulling out the suture after one hour.Each animal received drugs twice a day.Results48 hours after ischemia followed by 48 hours reperfusion,the ET-1 and IL-6 levels in both blood and brain tissue were significantly increased.Compared with ischemia-reperfusion group,these levels were significantly decreased in all hydroxyethylpuerarin-treated groups.ConclusionHydroxyethylpuerarin could protect neuronal injury induced by focal brain ischemia-reperfusion,probably through decreasing the synthesis and release of ET-1 or inflammatory reaction induced by some cytokines,such as IL-6.
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PurposeTo investigate the effect of hydroxyethylpuerarin on the levels of ET-1 and IL-6 in focal brain ischemia-reperfusion injury rats.MethodsRats were divided into 6 groups randomly,ie.sham-operate group,ischemia-reperfusion group,hydroxyethylpuerarin 15 mg/kg,30 mg/kg,60 mg/kg groups and nimodipine 0.2 mg/kg group.Rats were prepared with a model of focal brain ischemic injury by middle cerebral artery occlusion(MCAO),then recovered perfusion by pulling out the suture after one hour.Each animal received drugs twice a day.Results48 hours after ischemia followed by 48 hours reperfusion,the ET-1 and IL-6 levels in both blood and brain tissue were significantly increased.Compared with ischemia-reperfusion group,these levels were significantly decreased in all hydroxyethylpuerarin-treated groups.ConclusionHydroxyethylpuerarin could protect neuronal injury induced by focal brain ischemia-reperfusion,probably through decreasing the synthesis and release of ET-1 or inflammatory reaction induced by some cytokines,such as IL-6.
Key concepts: Nimodipine, Ischemia, Medicine, Reperfusion injury, Anesthesia, Perfusion, Middle cerebral artery, Internal medicine