动物造模,脑缺血再灌注损伤 z-bio 2022-07-21 401

　　Objective: To investigate the relationship between the protective effect of propofol on cerebral ischemia-reperfusion injury and gap junctions and its possible mechanism.

　　Methods: 70 male SD rats were randomly divided into sham operation (sham) group, ischemia-reperfusion (I/R) group, propofol low-dose (P25, 25 mg/kg) group, and medium-dose (P50, 50) group. mg/kg) group, high-dose (P100, 100 mg/kg) group, carbenoxolone (CBX) intervention ischemia-reperfusion (I/R+CBX) group, and carbenoxolone intervening propofol high-dose (P100+ CBX) group. The rat middle cerebral artery occlusion (MCAO) model was established by suture method, 2 h of cerebral ischemia and 24 h of reperfusion; the neurobehavioral score of rats was performed by Longa's method; the changes of cerebral infarction volume were detected by TTC staining; Western The protein expression changes of connexin 43 (Cx43), protein kinase C (PKC) and apoptosis-related factors Bax and Bcl-2 were detected by blot method.

　　Results: Compared with the ischemia-reperfusion group, except for the low-dose propofol group, the neurological deficit score and the percentage of cerebral infarction volume in the medium and high-dose propofol groups were significantly reduced, and the high-dose group had better effect; Peric acid can further enhance the protective effect of propofol on cerebral ischemia-reperfusion injury in rats. Western blot results showed that compared with the sham group, the expression of Cx43 protein and the ratio of Bax to Bcl-2 in the I/R group were significantly increased, while the expression of PKC protein was significantly decreased; The ratio of Bax to Bcl-2 was significantly decreased, and the expression of PKC protein was significantly increased; and carbenoxolone could enhance the effect of propofol.

　　Conclusion: Propofol pretreatment can alleviate I/R injury, and its mechanism may be related to the inhibition of gap junction function and the decrease of Bax/Bcl-2 ratio through PKC signaling pathway.