Objective: To investigate the effects of peoniflorin on cellular apoptosis of the rats with cerebral is-chemia reperfusion injury and its mechanism. Methods: Eighty SD rats were randomized into sham operation group, the model group, peoniflorin group and nimodipine group, 20 cases in each group, the rat model with cerebral is-chemia reperfusion injury was established, neurological behavior score and infarct area of the rats in different groups were observed, neural cell apoptosis of the rats were detected by TUNEL, the expressions of Bcl-2 and Bax protein were measured by immunohistochemical method. Results: The rats in the sham operation group didn't manifest the symptoms of nerve function impairment, the model group was higher than the sham operation group in neurological behavior score and infarct area obviously, peoniflorin group and nimodipine group were lower than the model group notably, and the difference showed statistical meaning (P<0.05); no nerve cellular apoptosis had been seen in the sham operation group, the model group was more than the sham operation group in TUNEL positive cells, peoni-florin group and nimodipine group were lower than the model group in the numbers of apoptotic cells and positive rates significantly, and the difference showed statistical meaning (P<0.05); gray levels of Bcl-2 and Bax in the sham operation group were higher than these of the model group, gray level of Bcl-2 decreased in peoniflorin group and nimodipine group compared with the model group, while Bax gray level raised obviously in both groups compared with the model group, and the difference demonstrated statistical meaning (P<0.05). Conclusion: Peoniflorin could inhibit the apoptosis of nerve cells by inhibiting the expressions of Bax and up regulating Bcl-2 expressions, thereby to protect nerve function and alleviate cerebral infarction.%目的：探讨芍药苷对大鼠脑缺血再灌注损伤细胞凋亡的影响及其作用机制。方法：选择健康雄性SD大鼠80只，随机分为假手术组、模型组、芍药苷组及尼莫地平组各20只，建立大鼠脑缺血再灌注损伤模型，观察各组大鼠神经行为学评分及脑梗死面积，TUNEL检测大鼠神经细胞凋亡情况，免疫组化法检测大鼠大脑皮层中Bcl-2和Bax蛋白表达情况。结果：假手术组大鼠未表现出神经功能缺失症状，模型组大鼠神经行为学评分及脑梗死面积高于假手术组，芍药苷组及尼莫地平组均低于模型组，差异具有统计学意义(P＜0.05)；假手术组几乎未见神经细胞凋亡，模型组TUNEL阳性细胞明显多于假手术组，芍药苷组及尼莫地平组细胞凋亡个数及阳性率均低于模型组，其差异具有统计学意义(P＜0.05)；假手术组大鼠大脑皮质中Bcl-2及Bax的灰度值均高于模型组，芍药苷组及尼莫地平组大鼠Bcl-2灰度值较模型组降低，而Bax灰度值较模型组明显升高，2组Bcl-2/ Bax灰度值较模型组下降，其差异具有统计学意义(P＜0.05)。结论：芍药苷可通过抑制Bax的表达，上调Bcl-2的表达来抑制神经细胞凋亡，从而保护神经功能，减轻脑梗死。
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