《Chinese Journal of Rehabilitation Theory and Practice》 ›› 2020, Vol. 26 ›› Issue (9): 1038-1044.doi: 10.3969/j.issn.1006-9771.2020.09.008

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Effects of Analgecine on Apoptosis and Neuroinflammation in Cerebral Ischemia-reperfusion Injury Rats

CHEN Xiao-ping,WANG Ming-yang,MA Deng-lei,GONG Shi-li,ZHANG Li,LI Ya-li,LI Lin,HU Chao-ying,ZHANG Lan()   

  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
  • Received:2019-12-24 Revised:2020-01-17 Published:2020-09-25 Online:2020-09-24
  • Contact: ZHANG Lan E-mail:lanizhg@126.com
  • Supported by:
    National Natural Science Foundation of China(81903880);Beijing High-level Health and Technical Personal Plan(2014-2-014);Capital Science and Technology Leading Talent Training Project(Z191100006119017);Beijing Hospitals Authority Ascent Plan(DFL20190803);Beijing Postdoctoral Research Foundation(2018-ZZ-105);China Postdoctoral Science Foundation(2019M650776)

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.

Key words: ischemic stroke, cerebral ischemia-reperfusion, Analgecine, motor, apoptosis, inflammation, rats