小窝蛋白Cav-1介导人参皂苷Rb1对小鼠脑缺血再灌注损伤的脑保护作用

doi:10.12092/j.issn.1009-2501.2020.03.004

中国临床药理学与治疗学 ›› 2020, Vol. 25 ›› Issue (3): 265-270.doi: 10.12092/j.issn.1009-2501.2020.03.004

小窝蛋白Cav-1介导人参皂苷Rb1对小鼠脑缺血再灌注损伤的脑保护作用

张高娇¹，王芯芯²，周佳²，王雷雷³，戴勤学³

¹温州市中西医结合医院麻醉科，²手术室，³温州医科大学附属第一医院麻醉科，温州 325000，浙江

收稿日期:2019-10-08 修回日期:2020-02-20 出版日期:2020-03-26 发布日期:2020-04-13
通讯作者: 戴勤学，男，硕士，主治医师，研究方向：围术期脏器保护。 Tel：13695842272 E-mail：653091408@qq.com
作者简介:张高娇，女，本科，主治医师，研究方向：围术期脏器保护。 Tel：18969766733 E-mail：423421864@qq.com
基金资助:
国家自然科学基金资助项目（81704180）；温州市科技局科技计划项目（Y20170143，Y20140543）

Ginsenoside Rb1 protects brain through Cav-1 for mice with cerebral ischemia-reperfusion injury

ZHANG Gaojiao ¹, WANG Xinxin ², ZHOU Jia², WANG Leilei ³, DAI Qinxue ³

¹Department of Anesthesiology, ² Operating Room, Wenzhou Hospital of Integrated Traditional Chinese and Western Medicine, Wenzhou 325000, Zhejiang, China; ³The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang, China

Received:2019-10-08 Revised:2020-02-20 Online:2020-03-26 Published:2020-04-13

摘要/Abstract

摘要： 目的:探讨小窝蛋白Cav-1介导人参皂苷Rb1对小鼠脑缺血再灌注损伤的脑保护作用。方法:将120只C57BL/6小鼠按随机数字表法分成假手术组、模型组、人参皂苷Rb1组、人参皂苷Rb1+Cav-1 siRNA组、人参皂苷Rb1+siNC组，每组24只。采用大脑中动脉闭塞（middle cerebral artery occlusion,MCAO）法建立小鼠脑缺血再灌注损伤模型。人参皂苷Rb1组在造模后即刻给予人参皂苷Rb1（40 mg/kg，i.p.），假手术组和模型组给予等量生理盐水。人参皂苷Rb1+Cav-1 siRNA组和人参皂苷Rb1+siNC组在造模前24 h分别侧脑室注射Cav-1 siRNA和siNC，其他操作同人参皂苷Rb1组。再灌注24 h时测各组小鼠神经行为学评分，然后每组各取6只小鼠分别检测脑组织含水量、脑梗死体积，大脑皮质半暗带区Cav-1 mRNA和Cav-1、Bcl2、Bax蛋白表达量。结果:与假手术组相比，模型组小鼠的神经行为学评分、脑梗死体积、脑组织含水量明显增加（P<0.05），Cav-1 mRNA和Cav-1蛋白表达量、Bcl-2/Bax比值明显减少（P<0.05）。与模型组相比，人参皂苷Rb1组小鼠的神经行为学评分、脑梗死体积、脑组织含水量明显减少，Cav-1 mRNA和Cav-1蛋白表达量、Bcl-2/Bax比值明显增加（P<0.05）；与人参皂苷Rb1组相比，人参皂苷Rb1+Cav-1 siRNA组神经行为学评分、脑梗死体积、脑组织含水量明显增加,且Cav-1 mRNA和Cav-1蛋白表达量、Bcl-2/Bax比值明显减少（P<0.05）。结论:人参皂苷Rb1对脑缺血再灌注损伤小鼠具有脑保护作用。而Cav-1 siRNA使小鼠脑组织中Cav-1蛋白表达下降后，可以明显逆转人参皂苷Rb1的脑保护作用，说明Cav-1蛋白介导了人参皂苷Rb1对脑缺血再灌注损伤小鼠的脑保护作用。

关键词: 脑缺血再灌注损伤, 人参皂苷Rb1, Cav-1, 神经保护

Abstract: AIM: To investigate the protective effect of ginsenoside Rb1 on brain through Cav-1 in mice with cerebral ischemia-reperfusion injury. METHODS: One hundred and twenty C57/B6 mice were randomly divided into sham operation group, model group, model + ginsenoside Rb1 group, ginsenoside Rb1+ Cav-1 siRNA group, ginsenoside Rb1+siNC group, 24 in each group. The model of cerebral ischemia-reperfusion injury in mice was established by middle cerebral artery occlusion (MCAO). The ginsenoside Rb1 group received intraperitoneally injection of ginsenoside Rb1 (40 mg/kg); the sham operation group and model group were intraperitoneally injected with an equal amount of physiological saline immediately after modeling. For the ginsenoside Rb1+ cav-1 siRNA group and the ginsenoside Rb1+siNC group, cav-1 siRNA and siNC were injected into the lateral ventricle 24 h before molding, respectively, and the other operations were the same as the ginsenoside Rb1 group. The neurobehavioral scores of the mice in each group were measured at 24 h after reperfusion, and the water content of brain tissue, cerebral infarction volume, Cav-1 mRNA and Cav-1, Bcl-2 and Bax protein expressions in the cerebral cortex penumbra were measured in each group. RESULTS:Compared with the sham operation group, the neurobehavioral scores, cerebral infarction volume and brain tissue water content in the model group were significantly increased (P<0.05), and the expressions of Cav-1 mRNA and Cav-1 protein, and the Bcl-2 /Bax ratio were significantly decreased (P<0.05). Compared with the model group, the neurobehavioral scores, cerebral infarction volume and brain tissue water content in the ginsenoside Rb1 group were significantly decreased, and the expressions of Cav-1 mRNA and Cav-1 protein, and the Bcl-2 /Bax ratio were significantly increased (P<0.05). Compared with the ginsenoside Rb1 group, the neurobehavioral scores, cerebral infarction volume and brain tissue water content in the ginsenoside Rb1 + cav-1 siRNA group were significantly increased, and the expressions of Cav-1 mRNA and Cav-1 protein, and the Bcl-2 /Bax ratio were significantly decreased (P<0.05). CONCLUSION: Ginsenoside Rb1 can protects brain for mice with cerebral ischemia-reperfusion injury. After Cav-1 siRNA decreased the expression of Cav-1 protein in the brain tissue of mice, it significantly reverses the cerebral protective effect of ginsenoside Rb1, indicating that Cav-1 protein mediated the cerebral protective effect of ginsenoside Rb1 on cerebral ischemia reperfusion injury mice.

Key words: brain ischemia reperfusion injury, ginsenoside Rb1, Cav-1, brain protection

中图分类号:

R965.2

张高娇，王芯芯，周佳，王雷雷，戴勤学. 小窝蛋白Cav-1介导人参皂苷Rb1对小鼠脑缺血再灌注损伤的脑保护作用[J]. 中国临床药理学与治疗学, 2020, 25(3): 265-270.

ZHANG Gaojiao, WANG Xinxin, ZHOU Jia, WANG Leilei, DAI Qinxue. Ginsenoside Rb1 protects brain through Cav-1 for mice with cerebral ischemia-reperfusion injury[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2020, 25(3): 265-270.

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小窝蛋白Cav-1介导人参皂苷Rb1对小鼠脑缺血再灌注损伤的脑保护作用

Ginsenoside Rb1 protects brain through Cav-1 for mice with cerebral ischemia-reperfusion injury

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