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探讨芍药苷对大鼠局灶性脑缺血再灌注脑血流量变化及PGI2/TXA2平衡的影响。取72只雄性SD大鼠,随机分为假手术组、I/R模型组、芍药苷(10、20及40 mg·kg-1)处理组以及尼莫地平组。线栓法制作大鼠局灶性脑缺血(90 min)/再灌注(24 h)模型。观察芍药苷对神经功能缺损评分及梗死体积的影响,采用激光多普勒血流仪监测给药前后大鼠缺血侧局部脑血流量的动态变化,免疫组化法检测缺血侧海马CA1区COX-2的表达;ELISA法测血清中血栓素A2(TXA2)和前列腺素I2(PGI2)含量并计算PGI2/TXA2比值。结果表明,芍药苷处理组较I/R模型组能显著改善神经功能缺损症状,缩小梗死体积,增加缺血侧大脑局部血流量,抑制COX-2阳性表达,降低TXA2含量,提高PGI2含量及PGI2/TXA2比值。结果提示,芍药苷对局灶性缺血大脑产生神经保护作用的机制可能与其改善缺血侧大脑血流供应,调节PGI2/TXA2平衡有关。
To investigate the effect of paeoniflorin on cerebral blood flow and the balance of PGI2 / TXA2 after focal cerebral ischemia / reperfusion in rats. Seventy-two male SD rats were randomly divided into sham operation group, I / R model group, paeoniflorin (10, 20 and 40 mg · kg -1) and nimodipine group. The model of focal cerebral ischemia (90 min) / reperfusion (24 h) was established by thread occlusion. To observe the effect of paeoniflorin on neurological deficit scores and infarct volume, the dynamic changes of ischemic regional cerebral blood flow before and after administration were monitored by laser Doppler flowmetry, the expression of paeoniflorin in hippocampal CA1 region The expression of COX-2, TXA2 and PGI2 in serum were detected by ELISA. The PGI2 / TXA2 ratio was calculated. The results showed that paeoniflorin treatment group than I / R model group can significantly improve the symptoms of neurological deficit, reduce infarct volume, increase ischemic local blood flow, inhibit COX-2 positive expression, reduce TXA2 content, increase PGI2 content and PGI2 / TXA2 ratio. The results suggest that the mechanism by which paeoniflorin exerts neuroprotection on focal ischemic brain may be related to the improvement of cerebral blood flow in ischemic side and the regulation of PGI2 / TXA2 balance.