摘要: 目的 探讨芍药苷对大鼠大脑中动脉阻塞 ( MCAO) 诱导的环

摘要: 目的 探讨芍药苷对大鼠大脑中动脉阻塞 ( MCAO) 诱导的环氧酶代谢通路表达的影响。
方法 ：120 只雄性 SD大鼠，随机分为假手术组、模型组、芍药苷低、中、高 ( 10、20、40 mg / kg) 剂量组、尼莫地平组。线栓法制作大鼠大脑中动脉缺血 90 min，再灌注 24 h 模型。观察芍药苷对神经症状、梗死体积及脑含水量的影响，采用免疫组化 SP法检测 COX-2 的表达情况，ELISA 法测缺血侧额区皮质肿瘤坏死因子-α ( TNF-α) 、白介素 1-β ( IL-1β) 、血栓素 A2（ TXA2 ) 和前列腺素 I2 ( PGI2 ) 水平。
结果 ：芍药苷处理组较模型组能显著改善大鼠神经缺损症状，缩小梗死体积，降低缺血侧脑含水量，抑制 COX-2 阳性表达，减少 TNF-α、IL-1β、TXA2 的释放，提高 PGI2 水平。
结论 ：芍药苷可能通过抑制花生四烯酸的环氧酶代谢通路产生脑神经保护作用。

結果 (英文) 1:

Abstract: the objective of paeoniflorin in rat Middle cerebral artery occlusion (MCAO)-induced expression of cyclooxygenase metabolic pathways.Methods: 120 male SD rats were randomly divided into the Sham-operated group, model groups, paeoniflorin in low, medium and high (10, 20, 40 mg/kg) dose group, Nimodipine group. Line method in the rat Middle cerebral artery ischemia and 90 min and 24 h of reperfusion model. Effects of paeoniflorin on neurological symptoms, infarction volume and brain water content in using immunohistochemical SP method to detect the expression of COX-2, ELISA method to measure the amount of ischemic cortex of tumor necrosis factor-α (TNF-α), Interleukin 1-β (IL-1 Beta), thromboxane A2 (TXA2) and prostaglandin I2 (PGI2) level.Results: paeoniflorin treatment group compared with the model groups can significantly improve symptoms of nerve defect in rats, reduced infarct volume, reduces ischemic brain water content, and inhibit the expression of COX-2, reduce TNF-alpha, IL-1 beta, the release of TXA2, increase PGI2.Conclusion: paeoniflorin by inhibiting cyclooxygenase arachidonic acid metabolic pathways of the brain protective effect.

結果 (英文) 2:

OBJECTIVE: To investigate the effect of cyclooxygenase pathway in the expression of paeoniflorin on cerebral artery occlusion (MCAO) induced.
Methods: 120 male SD rats were randomly divided into sham operation group, model group, paeoniflorin low, medium and high (10,20,40 mg / kg) dose group, nimodipine group. Suture method middle cerebral artery ischemia 90 min, 24 h after reperfusion model. To investigate the effects of paeoniflorin on neurological symptoms and cerebral infarct volume water content, using immunohistochemical SP method to detect the expression of COX-2, ELISA method to measure the amount of ischemic cortex tumor necrosis factor -α (TNF-α), interleukin-1-β (IL-1β) , thromboxane A2 (TXA2) and prostaglandin I2 (PGI2) level.
Results: paeoniflorin treatment group compared with the model group can significantly improve the neurological deficit symptoms in rats, reduced infarct size, reduce ischemic brain water content, inhibition of COX-2 expression, reduce TNF-α, IL-1β, TXA2 release, improve the level of PGI2.
Conclusion: paeoniflorin may have neuroprotective effect by inhibiting arachidonic acid cyclooxygenase pathways.

結果 (英文) 3:

Abstract: Objective To investigate the effect of the expression of the metabolic pathway induced by the middle cerebral artery occlusion (MCAO) in rats.Methods: 120 male SD rats were randomly divided into sham operation group, model group, low, middle, high (20, 10, 40 mg / kg) dose group and nimodipine group. The rat middle cerebral artery ischemia 90 min was made by thread embolism method, and then 24 h reperfusion model was made. To observe the effect of paeoniflorin content on cerebral infarction volume and neurological symptoms, the expression of SP was detected by immunohistochemistry COX-2, alpha measured in ischemic frontal cortex tumor necrosis factor - ELISA (TNF- alpha), interleukin 1- beta (IL-1 beta), thromboxane A2 (TXA2) and prostaglandin I2 (PGI2) level.Results: the treatment group than the control group, paeoniflorin can significantly improve symptoms of nerve defect in rats, reduce infarct volume, reduce ischemic brain water content, inhibiting the positive expression of COX-2, TNF- alpha, IL-1 beta, reduce the release of TXA2, increase the level of PGI2.Conclusion: it is possible to protect the brain by inhibiting the metabolic pathway of arachidonic acid in four.