脑缺血再灌注损伤 z-bio 2021-07-07 634

　　Objective: Based on the Rho/Rho-kinase signaling pathway to study the effect of propofol on reducing cerebral ischemia-reperfusion injury in rats.

　　Method: 100 SD rats were divided into control group, model group, low, medium and high dose propofol (20.0, 40.0, 80.0 mg/kg), model, low, medium and high dose propofol group. A model of ischemia-reperfusion injury was established. After successful modeling, the low, medium, and high-dose propofol groups were orally given corresponding doses of propofol. The control group and the model group were given the same amount of normal saline for 4 weeks. Finally, the neuropathy of each rat was scored, the stickers were removed and the balance beam walking experiment was performed, and the hippocampus of the rats was scored pathologically. At the same time, we recorded the levels of ho and Rho kinase mRNA and protein in the brain. Measure rat tissue.

　　Results: The hippocampal neurological deficit score, bilateral sticker removal time, balance beam crossing time, hippocampal histopathological score, and Rho and Rho kinase mRNA and protein expression levels in the model group were averaged in the control group (P). u003c0.05); Propofol each dose group nerve defect score, bilateral sticker removal time, balance beam crossing time, hippocampal histopathology score, brain tissue hippocampus Rho, Rho kinase mRNA and protein expression levels are compared with the lower group of the model More significant (P u003c0.05); and with the increase of propofol dose, nerve defect score, bilateral stick removal time, balance beam crossing time, hippocampal tissue pathology score, and Rho and Rho expression levels in brain tissue-hippocampal kinase mRNA and protein gradually decreased. The relationship between dose and effect is clear (Pu003c0.05). The hippocampal neurons in the control group were complete and well positioned. In the model group, the hippocampal neurons were loosely arranged, the cells were deeply stained and pyknotic, there was flaky necrosis, and the interstitial neurons were separated. Neurons in the high-dose propofol group tended to be normal. Compared with the model group, the nerve cells in the middle and low-dose propofol groups were looser and less pyknotic, and the neurons in the neurons were clearly visible.

　　Conclusion: Propofol can reduce the nerve damage caused by cerebral ischemia and reperfusion in rats. The mechanism is related to propofol inhibiting the expression of Rho and Rho-kinase mRNA and protein, and activating the Rho/Rho-kinase signal pathway.