动物造模,脑缺血再灌注损伤 z-bio 2022-03-18 366

　　Objective To investigate the effect of propofol on reducing cerebral ischemia-reperfusion injury in rats based on Rho/Rho-kinase signaling pathway.

　　Methods 100 SD rats were divided into control group, model group, propofol low, medium and high dose groups (20.0, 40.0, 80.0 mg/kg), model group, propofol low, medium and high dose groups to establish brain The ischemia-reperfusion injury model was established. After the modeling was successful, propofol low, medium and high dose groups were given corresponding doses of propofol by gavage, and the control group and model group were given an equal volume of normal saline for 4 weeks. , Each rat was scored for neurological deficit, the sticker removal and balance beam walking experiments were performed, the pathological score was performed on the hippocampus of the rat, and the levels of Rho, Rho-kinase mRNA and protein in the rat brain tissue were determined at the same time.

　　Results The neurological deficit score, bilateral sticker removal time, balance beam passing time, hippocampal histopathological score, Rho, Rho-kinase mRNA and protein expression levels in the brain tissue hippocampus in the model group were significantly higher than those in the control group (P<0.05); C The neurological deficit score, bilateral sticker removal time, balance beam passing time, hippocampal histopathological score, and mRNA and protein expression levels of Rho and Rho-kinase in the hippocampus of brain tissue in each dose group of pofol were significantly lower than those in the model group (P<0.05). ;And with the increase of propofol dose, the neurological deficit score, bilateral sticker removal time, balance beam passing time, hippocampal histopathological score, Rho, Rho-kinase mRNA and protein expression levels in the hippocampus of brain tissue gradually decreased , the dose-effect relationship was significant (P<0.05). In the control group, the neurons in the hippocampus were intact and tightly arranged; in the model group, the neurons in the hippocampus were loosely arranged, with hyperchromatic pyknosis, sheet-like necrosis, and interstitial isolation of neurons; in the high-dose propofol group, the neurons tended to be normal. ;Compared with the model group, the propofol medium and low dose groups had less loose nerve cells and less pyknosis, and the nucleoli of neuron cells were clearly visible.

　　Conclusion Propofol can alleviate the neurological damage of cerebral ischemia-reperfusion in rats; the mechanism is related to that propofol can inhibit the expression of Rho, Rho-kinase mRNA and protein and then inhibit the activation of Rho/Rho-kinase signaling pathway.