Neuroprotective effect of Paeoniae Radix Rubra on hippocampal CA1 region of mice induced by transient focal cerebral ischemia via anti-gliosis and anti-oxidant activity

被引:0
作者
Xiao-lu Zhu [1 ,2 ]
Bing-chun Yan [1 ,3 ,4 ]
Cheng Tang [1 ]
Guo-wei Qiu [1 ]
Yao Wu [1 ]
Jie Wang [1 ]
Ping Bo [1 ]
机构
[1] Department of Traditional Chinese and Western Medicine, Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou University
[2] Medical Center, Yangzhou University
[3] Jiangsu Key Laboratory of Zoonosis, Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses,Yangzhou University
[4] Department of Neurology, Affiliated Hospital, Yangzhou University
基金
中国博士后科学基金;
关键词
cerebral ischemia/reperfusion; gliosis; neuroprotective; oxidative stress; Paeoniae Radix Rubra;
D O I
暂无
中图分类号
R285.5 [中药实验药理];
学科分类号
1008 ;
摘要
Objective: Stroke is the second leading cause of death worldwide. This study aimed to investigate the neuroprotective effect of Paeoniae Radix Rubra(PRR) on ischemic stroke of mice.Methods: The focal ischemic stroke model was produced via middle cerebral artery occlusion. The experimental mice were divided into four groups: vehicle-sham group, PRR-sham group, vehicle-ischemia group, and PRR-treated ischemia group. The cerebral infarction volume was detected with TTC staining.The number of neurons in the hippocampal CA1 of the ischemic side, and the activation of astrocytes and microglia were observed via immunohistochemical staining. Western blotting was used to determine the expression changes of SOD1, SOD2, and Catalase protein levels in the hippocampus.Results: PRR significantly reduced the cerebral infarct volume induced by ischemic injury and inhibited the astrocytes and microglia activation in the hippocampal CA1 region. The decreased levels of SOD1,SOD2, and Catalase that was induced by ischemic reperfusion were simultaneously improved after PRR treatment.Conclusion: PRR improved neuronal injuries that were induced by transient cerebral ischemia via inhibiting gliosis and elevating anti-oxidants.
引用
收藏
页码:86 / 91
页数:6
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