[1]张红艳,翟 丽,王婷婷,等.胡黄连苷Ⅱ通过抑制cyto C/caspase-9/caspase-3通路发挥神经保护作用[J].中国药理学通报,2017,(05):668-674.[doi:10.3969/j.issn.1001-1978.2017.05.016]
 ZHANG Hong-yan,ZHAI Li,WANG Ting-ting,et al.Picroside Ⅱ plays a neuroprotective effect by inhibiting cyto C/caspase-9/caspase-3 signal pathway following ischemia/reperfusion injury in rats[J].Chinese Pharmacological Bulletin,2017,(05):668-674.[doi:10.3969/j.issn.1001-1978.2017.05.016]
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胡黄连苷Ⅱ通过抑制cyto C/caspase-9/caspase-3通路发挥神经保护作用()
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《中国药理学通报》[ISSN:/CN:]

卷:
期数:
2017年05期
页码:
668-674
栏目:
论著
出版日期:
2017-05-15

文章信息/Info

Title:
Picroside Ⅱ plays a neuroprotective effect by inhibiting cyto C/caspase-9/caspase-3 signal pathway following ischemia/reperfusion injury in rats
文章编号:
1001-1978(2017)05-0668-07
作者:
张红艳翟 丽王婷婷李 珊张艳辉郭云良
青岛大学附属医院脑血管病研究所,山东 青岛 266003
Author(s):
ZHANG Hong-yan ZHAI Li WANG Ting-ting LI Shan ZHANG Yan-hui GUO Yun-liang
Institute of Cerebrovascular Diseases, Affiliated Hospital of Qingdao University, Qingdao Shandong 266003,China
关键词:
胡黄连苷Ⅱ 缺血/再灌注损伤 cyto C/caspase-9/caspase-3信号通路 神经保护 大鼠
Keywords:
picroside Ⅱ cerebrum ischemic/reperfusion injury cyto C/caspase-9/caspase-3 signal pathway neuroprotection rats
分类号:
R-332;R284.1;R322.81;R329.25;R743.310.22;R977.6
DOI:
10.3969/j.issn.1001-1978.2017.05.016
文献标志码:
A
摘要:
目的 研究胡黄连苷Ⅱ对大鼠脑缺血/再灌注过程中cyto C/caspase-9/caspase-3信号通路的影响及其神经保护作用机制。方法 环孢素(CsA)和苍术苷(Atr)分别作为cyto C阳性对照和阴性对照,改良Longa法制备缺血2 h再灌注24 h大鼠脑缺血/再灌注(I/R)模型。再灌注24 h后,TTC染色观察脑梗死体积; 免疫组织化学和Western blot检测cyto C、caspase-9、caspase-3表达水平。结果 模型组大鼠脑缺血/再灌注后TTC显示染色脑梗死体积明显增加; 免疫组织化学和Western blot显示cyto C、caspase-9、caspase-3表达水平较假手术组明显增多(P<0.05)。治疗组大鼠TTC显示脑梗死体积缩小; 免疫组化和Western blot显示cyto C、caspase-9、caspase-3表达水平与模型组相比明显降低(P<0.05)。与Atr组相比,Atr+胡黄连苷Ⅱ组大鼠脑梗死体积缩小,免疫组化和Western blot显示cyto C、caspase-9、caspase-3表达水平减弱(P<0.05)。结论 胡黄连苷II抑制缺血/再灌注损伤大脑神经凋亡的机制可能与下调cyto C/caspase-9/caspase-3信号通路蛋白有关。
Abstract:
Aim To investigate the neuroprotective effect of picroside Ⅱ(PIC)on cyto C/caspase-9/caspase-3 signal pathway following ischemia/reperfusion(I/R)injury in rats.Methods Atractyloside(Atr)was selected as negative control, cyclosporin A(CsA)was selected as positive control, and PIC was selected as the treatment medicine.The I/R model was made by inserting a monofilament suture into internal carotid artery for 2 h, and then reperfused for 24 h.The cerebral infarction volume was detected by TTC staining, and the expression of cyto C, caspase-9 and caspase-3 were determined by immunohistochemical assay and Western blot.Results In model group, the cerebral infarct volume was obviously large; the expression of cyto C, caspase-9 and caspase-3 was increased significantly more than that in sham group(P<0.05).In PIC group, the cerebral infarct volume was significantly improved; the expression of cyto C, caspase-9 and caspase-3 was significantly decreased than that in model group(P<0.05).In Atr+PIC group, the rat infarction volume was reduced, and the expression of cyto C, caspase-9 and caspase-3 was significantly decreased than that in Atr group(P<0.05).Conclusion The mechanism of PIC inhibiting neuron apoptosis in focal cerebral I/R rats might be through down-regulating the expression of cyto C, caspase-9 and caspase-3.

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备注/Memo

备注/Memo:
基金项目:国家自然科学基金资助项目(No 81274116)
作者简介:张红艳(1989-),女,硕士生,研究方向:脑血管病,E-mail:1042022747@qq.com;
郭云良(1961-),男,博士,教授,博士生导师,研究方向:脑血管病,通讯作者,E-mail:guoqdsd@163.com
更新日期/Last Update: 2017-05-15