Protective effect of propofol against cerebral ischemic/reperfusion injury may involve inhibition of gap junction
10.3969/j.issn.1673-4254.2015.12.03
- VernacularTitle:丙泊酚保护脑缺血再灌注损伤可能与缝隙连接功能的抑制相关
- Author:
Zongbing FAN
1
;
Xuhui TONG
;
Yan LI
;
Li YU
;
Yinling CHEN
;
Haoang LIU
;
Shuying DONG
Author Information
1. 蚌埠医学院药学系药理学教研室
- Keywords:
cerebral ischemia reperfusion injury;
propofol;
PKC;
Cx43;
gap junction;
apoptosis
- From:
Journal of Southern Medical University
2015;(12):1678-1682
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect of propofol against focal cerebral ischemia/reperfusion (I/R) injury in rats and its relation with gap junction. Methods Seventy adult male SD rats were randomly divided into sham-operated group, I/R group, low-, moderate-, and high-dose propofol groups (25, 50, 100 mg/kg;P25, P50, P10 groups, respectively), I/R+CBX group and P10+CBX group. Thread occlusion was used to induce middle cerebral artery occlusion (MCAO) in the mice for 2 h followed by reperfusion for 24 h. Longa's scores were used to evaluate the neurological behavior of the rats. TTC staining was used to measure the cerebral infarction volume and Western blotting was performed to detect the expressions of Cx43, PKC, Bax, and Bcl-2 in the brain of the rats. Results Compared with the I/R group, the rats pretreated with moderate and high doses of propofol showed significantly reduced neurological behavior scores and cerebral infarction volume percentage, and the effect was more obvious in high-dose propofol pretreatment group. CBX obviously enhanced the protective effect of propo-fol against I/R injury. Compared with those in the sham-operated group, the protein expression of Cx43 and the Bax/Bcl-2 ratio were increased and the protein expression of PKC was reduced in I/R group, and these changes were significantly reversed by high-dose propofol pretreatment;the effects of propofol were further enhanced by CBX. Conclusion The protective effect of propofol against cerebral I/R injury may involve the inhibition of the gap junction via PKC signaling and by reducing the Bax/Bcl-2 ratio.
