Effects of Analgecine on Apoptosis and Neuroinflammation in Cerebral Ischemia-reperfusion Injury Rats
10.3969/j.issn.1006-9771.2020.09.008
- VernacularTitle:痘苗病毒致炎兔皮提取物对脑缺血再灌注脑损伤大鼠凋亡和神经炎症的影响
- Author:
Xiao-ping CHEN
1
;
Ming-yang WANG
1
;
Deng-lei MA
1
;
Shi-li GONG
1
;
Li ZHANG
1
;
Ya-li LI
1
;
Lin LI
1
;
Chao-ying HU
1
;
Lan ZHANG
1
Author Information
1. Department of Pharmacy, Xuanwu Hospital Capital Medical University, National Clinical Research Center for Geriatric Diseases, Beijing Engineering Research Center for Nervous System Drugs, Key Laboratory for Neurodegenerative Diseases of Ministry of Education, Beijing 100053, China
- Publication Type:Research Article
- Keywords:
ischemic stroke;
cerebral ischemia-reperfusion;
Analgecine;
motor;
apoptosis;
inflammation;
rats
- From:
Chinese Journal of Rehabilitation Theory and Practice
2020;26(9):1038-1044
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the effects of Analgecine (AGC) on middle cerebral artery ischemia-reperfusion injury in rats and its mechanism. Methods:A total of 61 Sprague-Dawley rats were divided into sham group (n = 11), sham-AGC group (n = 11), model group (n = 20) and model-AGC group (n = 19). The model group and the model-AGC group were occluded the middle cerebral arteries for 1.5 hours and reperfused (2 rats in each group unsuccessful). The sham-AGC group and the model-AGC group were injected AGC 20 U/kg through tail-vein, while the sham group and the model group were injected saline of same volume. Four rats in each group were tested heat shock proteins 70 (HSP70), Bcl-2 and Bax in brain with Western blotting 48 hours after injection. The other rats were assessed with Prehensile Traction Test seven days after injection, and then, four of each group were detected ionized calcium binding adapter molecule 1 (Iba1) and glial fibrillary acidic protein (GFAP) expression with immunohistochemistry. Results:The prehensile time increased in the model-AGC group compared with that of the model group (P < 0.01), with the increase of HSP70 and Bcl-2 (P < 0.01) and decrease of Iba1 and GFAP expression (P < 0.05). Conclusion:AGC may promote the recovery of motor function in rats with cerebral ischemia-reperfusion injury, which may associate with inhibiting cell apoptosis and neruoinflammatory response.
