关键词: 异丙酚, 脑缺血/再灌注损伤, 神经保护

Abstract: Objective To investigate whether propofol pretreatment can reduce neurological damage induced by focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods A rat middle cerebral artery occlusion (MCAO) model was established to induce focal cerebral ischemia. Rats were randomly assigned to four groups (n=12 per group): sham, MCAO, propofol, and propofol + ErbB4 antagonist (propofol + PD158780). Neurological function was evaluated using the neurological severity score (NSS), infarct volume was measured by TTC staining, neuronal pathological morphology was assessed by HE staining microscopy and Bcl-2 protein content was quantified by Western blot. Results Compared to sham controls, MCAO group exhibited significantly higher NSS scores (P＜0.05), larger cerebral infarction volume (P＜0.05), and more severe neuronal damage in the cerebral cortex (P＜0.05), while the expression of Bcl-2 protein in brain tissue remained unchanged(P＞0.05).Compared to the MCAO group, the propofol group exhibited significantly lower NSS scores (P＜0.05), reduced infarct volume(P＜0.05), alleviated neuronal damage in the cerebral cortex (P＜0.05), and significantly increased Bcl-2 expression (P＜0.05). Compared to the propofol group, the propofol+PD158780 group demonstrated significantly increased NSS scores (P＜0.05), larger infarct volume (P＜0.05), aggravated neuronal damage (P＜0.05), and decreased Bcl-2 expression (P＜0.05). Conclusions Propofol pretreatment may attenuate cerebral I/R-induced neurological damage via the Nrg-1β/ErbB4 signaling pathway.

Key words: propofol, cerebral ischemia/reperfusion injury, neuroprotection