[Animal modeling]-Propofol's protection from cerebral ischemia-reperfusion injury may be related to the inhibition of gap junction function

  Objective: To explore the protective effect of propofol on cerebral ischemia-reperfusion injury and gap junction and its possible mechanism.

  Methods: 70 male SD rats were randomly divided into sham operation (pseudo) group, ischemia-reperfusion (I/R) group, propofol low-dose (P25, 25mg/kg) group, middle-dose (P50, 50mg/ kg)) is divided into kilograms). ) Group, high-dose (P100, 100 mg/kg) group, phenoxyketone (CBX) intervention ischemia-reperfusion (I/R+CBX) group, phenoxyketone intervention high-dose propofol (P100+CBX)) group. The middle cerebral artery embolism (MCAO) rat model was prepared by suture, cerebral ischemia for 2 hours, and reperfusion for 24 hours. The Longa method was used for neurobehavioral scoring of rats. TTC staining is used to detect changes in cerebral infarct volume. Western blotting is used to detect changes in the expression of connexin 43 (Cx43), protein kinase C (PKC), and apoptosis-related factors Bax and Bcl-2 proteins.

  Result: Except for the low-dose propofol group, compared with the ischemia-reperfusion group, the ratio of neurological deficit score and cerebral infarction volume in the middle and high-dose propofol groups was significantly reduced, and the high-dose group was significantly reduced. More effective; Phenoxyketone 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 Cx43 protein expression and the ratio of Bax to Bcl-2 in the I/R group were significantly increased, and the PKC protein expression was significantly reduced. In the I/R group, the expression of Cx43 protein and the ratio of BaxBcl-2 to Bcl-2 were significantly reduced, and the expression of PKC protein was significantly increased. Carbenoxolone can enhance the effectiveness of this propofol.

  Conclusion: Propofol pretreatment can alleviate I/R injury. The mechanism is related to the inhibition of gap junction function through PKC signaling pathway and the reduction of Bax/Bcl-2 ratio. It is possible.