Chinese Journal of Pharmacovigilance ›› 2016, Vol. 13 ›› Issue (12): 708-711.

• Orginal Article • Previous Articles     Next Articles

Exploration on Reasonable Prescription of Guhong Injection in Improving Mitochondrial Function of Cerebral Ischemia-reperfusion Rats

FENG Lu1, ZUO Ping-ping1, *, WANG Ming-yang1, YANG Nan1, FAN Si-yuan2, CUI Li-ying2   

  1. 1 Department of Pharmacology, Institute of Basic Medical Sciences, Beijing 100005, China;
    2 Department of Neurology, Peking Union Medical College Hospital /Chinese Academy Medical Sciences, Beijing 100005, China
  • Received:2017-01-13 Revised:2017-01-13 Online:2016-12-20 Published:2017-01-13

Abstract: Objective To explore the difference of the expression of autophagy related proteins between Guhong injection and its main components acetylglutamine and safflower in rats with cerebral ischemia reperfusion injury. Methods The middle cerebral artery occlusion (MCAO) model of SD rats was made by thread embolization. The rats were randomly divided into sham operation group, model group, acetylglutamine group, safflower group and Guhong group (n = 8). Behavioral tests (modified Neurological Severity Score and adhesive-removal test) were performed at 14 d after MCAO. The expressions of Beclin1, Parkin, KIFC2 and UCP3 were detected by Western blot. Results Significant changes in Neurological Severity Score, somatosensory and motor behavior were found in model animals, but there were no obvious change in the groups of acetylglutamate and safflower. The treatment of Guhong could effectively reverse cortical mitochondria and autophagy function of the above-mentioned protein expression changes in ischemic rats (P <0.01), while the acetylglutamine group and safflower group had no significant change. Conclusion The effect of Guhong injection on function of mitochondria of cerebral ischemia reperfusion injury in rats was significantly stronger than acetylglutamine injection and safflower injection.

Key words: Guhong injection, acetylglutamine, safflower, brain ischemia, mitophagy

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