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北五味子总木脂素对脑缺血模型大鼠神经细胞凋亡及p-AKT表达的影响
引用本文:姜恩平,王帅群,王卓,于春荣,陈建光,于春艳. 北五味子总木脂素对脑缺血模型大鼠神经细胞凋亡及p-AKT表达的影响[J]. 中国中药杂志, 2014, 39(9): 1680-1684
作者姓名:姜恩平  王帅群  王卓  于春荣  陈建光  于春艳
作者单位:北华大学 药学院, 吉林 吉林 132001;广东医学院, 广东 东莞 523808;北华大学 药学院, 吉林 吉林 132001;吉林市中心医院, 吉林 吉林 132001;吉林市中心医院, 吉林 吉林 132001;北京昭衍新药研究中心股份有限公司, 北京 100176;北华大学 药学院, 吉林 吉林 132001;北华大学 基础医学院, 吉林 吉林 132001
基金项目:吉林省教育厅项目(2011130,2012394);广东医学院博士启动项目(B2012063);吉林省科技厅项目(201215103)
摘    要:目的:观察北五味子总木脂素(Schisandra chinensis lignans,SCL)对局灶性脑缺血损伤大鼠神经细胞凋亡和PI3K/AKT信号传导途径的影响,并探讨其作用机制。方法:用北五味子总木脂素高、中、低剂量组(100,50,25 mg·kg-1)给大鼠分别灌胃给药,连续14 d后,线栓法建立脑缺血损伤模型,进行神经功能评分,TTC染色观察大鼠的脑梗死面积,HE染色观察脑组织的病理形态学改变,免疫组化检测脑组织中Bcl-2和Bax的表达,Western blotting检测脑组织内p-AKT和AKT蛋白的表达情况。结果:与模型组比较,北五味子总木脂素高、中、低剂量组均能不同程度缩小脑梗死面积;改善脑组织的病理形态学改变;促进抗凋亡蛋白Bcl-2的表达,抑制促凋亡蛋白Bax表达,同时促进p-AKT的表达。结论:北五味子总木脂素对大鼠脑缺血性损伤具有一定的保护作用,机制可能与其促进p-AKT活性增加,提高脑组织抗缺血损伤的能力和抑制神经细胞的凋亡有关。

关 键 词:五味子  脑缺血  磷脂酰肌醇3激酶  凋亡
收稿时间:2013-10-15

Effect of Schisandra chinensis lignans on neuronal apoptosis and p-AKT expression of rats in cerebral ischemia injury model
JIANG En-ping,WANG Shuai-qun,WANG Zhuo,YU Chun-rong,CHEN Jian-guang and YU Chun-yan. Effect of Schisandra chinensis lignans on neuronal apoptosis and p-AKT expression of rats in cerebral ischemia injury model[J]. China Journal of Chinese Materia Medica, 2014, 39(9): 1680-1684
Authors:JIANG En-ping  WANG Shuai-qun  WANG Zhuo  YU Chun-rong  CHEN Jian-guang  YU Chun-yan
Affiliation:College of Pharmacy, Beihua University, Jilin 132001, China;Guangdong Medical College, Dongguan 523808, China;College of Pharmacy, Beihua University, Jilin 132001, China;Jilin Central General Hospital, Jilin 132001, China;Jilin Central General Hospital, Jilin 132001, China;JOINN Laboratories, Beijing 100176, China;College of Pharmacy, Beihua University, Jilin 132001, China;Basic Medical College, Beihua University, Jilin 132001, China
Abstract:Objective: To observe the effect of Schisandra chinensis lignans(SCL) on neuronal apoptosis and PI3K/AKT signaling pathway of rats in the cerebral ischemia injury model, and study its possible mechanism.Method: Rats were orally administered SCL high, middle and low dose groups (100, 50, 25 mg·kg-1) for 14 days.The cerebral ischemia injury model was established by using the suture-occluded method to rate the neurological functions.The cerebral infarction area was observed by TTC staining.The pathological changes in brain tissues were determined by HE staining.Bcl-2 and Bax expressions were detected by immunohistochemical assay.The protein expressions of p-AKT and AKT were assayed by Western blotting.Result: Compared with the model group, SCL high, middle and low dose groups showed reduction in the cerebral infarction area to varying degrees, improve the pathological changes in brain tissues, promote the expression of apoptin Bcl-2 and p-AKT, and inhibit the expression of apoptin Bax.Conclusion: SCL shows a protective effect on rats with cerebral ischemia injury.Its mechanism may be related to the increase in p-AKT ability and anti-ischemic brain injury capacity and the inhibition of nerve cells.
Keywords:Schisandra chinensis  cerebral ischemia  phosphatidylinositol 3-kinase  apoptosis
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