Objective: The purpose of this paper was to study the protective effect of paeoniflorin on acute cerebral ischemia. The animal model of cerebral infarction induced by Middle Cerebral Artery Occlusion (MCAO) was blocked by the suture method. Sixty SD rats were randomly divided into the shame group, MCAO group, paeoniflorin (60, 120, 240 mg/kg, respectively) and Nimodipine (NMDP) group (n = 10 per group).

Methods: The rats were intragastrically administered immediately after the operation. After 7 days of gavage, the brains were decapitated at 24 h. Hematoxylin and Eosin (HE) staining was used to observe the degree of cell damage in the cerebral cortex of rats. Immunohistochemistry was used to detect silver plating and to observe changes in nerve cells. Rats in the model group showed obvious symptoms of neurological deficits, such as the ischemic morphological changed, the Malondialdehyde (MDA), Lactate Dehydrogenase (LD) content and lactate dehydrogenase (LDH) activity were significantly increased in the ischemic brain tissue, while the Superoxide Dismutase (SOD) activity was decreased.

Results: The decrease in Na+-K+-ATPase activity was significantly lower than that in the sham group. The neurological symptoms and signs of MCAO in the different doses of paeoniflorin group were improved, and the neuronal edema in the cortical area was alleviated. The activities of SOD, LDH and Na+-K+-ATPase were significantly increased, and the contents of MDA and LD were decreased.

Conclusion: Therefore, paeoniflorin could alleviate the degree of tissue damage in rats with acute cerebral infarction, inhabit the formation of free radicals in the brain tissue after ischemia, and reduce the degree of lipid peroxidation. Thus, the degree of cell damage was reduced greatly and a protective effect was showed on cerebral ischemia.

目的：研究of药苷对急性脑缺血的保护作用。用缝合法阻断由中脑动脉闭塞（MCAO）引起的脑梗死的动物模型。60只SD大鼠随机分为耻辱组，MCAO组，pa药苷（分别为60、120、240 mg / kg）和尼莫地平（NMDP）组（每组n = 10）。

方法：大鼠在手术后立即进行胃内给药。灌胃7天后，在24小时内将大脑断头。使用苏木精和曙红（HE）染色观察大鼠大脑皮层中细胞的损伤程度。免疫组织化学用于检测镀银并观察神经细胞的变化。模型组大鼠表现出明显的神经功能缺损症状，如缺血形态改变，缺血性脑组织中丙二醛（MDA），乳酸脱氢酶（LD）含量和乳酸脱氢酶（LDH）活性显着增加，而超氧化物歧化酶歧化酶（SOD）活性降低。

结果：Na + -K + -ATPase活性的降低明显低于假手术组。pa药苷不同剂量组MCAO的神经症状和体征得到改善，皮质区神经元水肿得到缓解。SOD，LDH和Na + -K + -ATPase的活性显着增加，MDA和LD的含量降低。

结论：pa药苷可减轻急性脑梗死大鼠的组织损伤程度，促进缺血后脑组织中自由基的形成，降低脂质过氧化程度。因此，细胞损伤的程度大大降低，并显示出对脑缺血的保护作用。