Protective Effect of Paeoniflorin on Acute Cerebral Infarction in Rats

芍药苷 医学 丙二醛 乳酸脱氢酶 超氧化物歧化酶 缺血 脑损伤 脑梗塞 H&E染色 水肿 药理学 内科学 梗塞 内分泌学 麻醉 免疫组织化学 化学 氧化应激 生物化学 心肌梗塞 酶 高效液相色谱法 色谱法
作者
Weilin Wu,Chenfeng Qiu,Xuewen Feng,Xiaoxiao Tao,Qian Zhu,Zhengjun Chen,Xiaomin Ma,Jinwei Yang,Xian-Jun Bao
出处
期刊:Current Pharmaceutical Biotechnology [Bentham Science Publishers]
卷期号:21 (8): 702-709 被引量:20
标识
DOI:10.2174/1389201021666191224151634
摘要

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.
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