Effects of salidroside on expression of NeuN and Egr4 in ischemic side of MCAO rats by inhibiting expression of C3
10.3969/j.issn.1001-1978.2017.11.020
- VernacularTitle:红景天苷通过抑制补体C3的表达对MCAO大鼠缺血侧NeuN、Egr4影响的研究
- Author:
ying Bai SONG
1
;
fang Wen LAI
;
qing Yan SU
;
Yu LIN
;
Wen XU
;
zhu Gui HONG
Author Information
1. 福建中医药大学药学院
- Keywords:
salidroside;
cerebral ischemia-reperfusion;
complement C3;
C3aR inhibitor;
Egrs;
neuro-protection
- From:
Chinese Pharmacological Bulletin
2017;33(11):1579-1584
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effects of salidroside on NeuN and Egrs in the ischemic side of middle cerebral artery occlusion (MCAO) rats by inhibiting complement C3.Methods The rats were subjected to MCAO with suture-occluded method,and the neurologic injury was evaluated.The rats underwent l h ischemia/reperfusion with 1 d and 2d salidroside treatment,and the expressions of NeuN,Egr4,C3 and C1 were tested.Male Sprague Dawley rats were separately injected ventricle C3aR inhibitor and artificial cerebrospinal fluid with the help of ventricle stereotaxic apparatus.Thirty min later,the models of MCAO were finished with 1h reperfusion,drug administration and intracerebroventricular injection for 2d.The expressions of NeuN,Egr4,C3 were detected.Results Compared with models of MCAO,the expression of C3 in MCAO rats treated with salidroside 1 d and 2d decreased significantly,and the expression of NeuN increased markedly.Salidroside had no apparent effect on Egr4 and C1 of administration of 1d,but it could significantly enhance the expression of Egr4 after 2d,and reduce the expression of C1 significantly after 2d.The rats administrated with C3aR inhibitor into cerebral ventricle continueously showed the same result in accordance with the treatment of salidroside.And the treatment of salidroside and C3aR inhibitor did not show remarkable additive effects.Conclusion The neuroprotective effect of salidroside on acute cerebral ischemia/reperfusion injury may be related to the inhibition of the activation of the classical pathway of complement,the regulation of Egrs and the reduction of apoptosis.
