Journal of Southern Medical University ›› 2015, Vol. 35 ›› Issue (12): 1678-.

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Protective effect of propofol against cerebral ischemic/reperfusion injury may involve
inhibition of gap junction

FAN Zongbing, TONG Xuhui, LI Yan, YU Li, CHEN Yinling, LIU Haoang, DONG Shuying   

  • Online:2015-12-20 Published:2015-12-20

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, P100 groups, respectively), I/R+
CBX group and P100+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 propofol
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.