中国药业2026，Vol.35Issue(8)：64-70,7.DOI:10.3969/j.issn.1006-4931.2026.08.012
丙泊酚抑制体外循环模型大鼠神经细胞凋亡机制研究
Study on the Mechanism of Propofol Inhibiting Neuronal Apoptosis in the Rat Model of Cardiopulmonary Bypass
摘要
Abstract
Objective To investigate the effect of propofol on hippocampal neuronal apoptosis in the rat model of cardiopulmonary bypass(CPB).Methods A rat model of CPB was established by intubation.A total of 60 rats were randomly divided into control group(equal volume of normal saline),model group(equal volume of normal saline),dexmedetomidine group(5 µg/kg),and low-,medium-,and high-dose propofol groups(10,20,40 mg/kg),with 10 rats in each group.Neurological impairment was assessed using the modified neurological severity score(mNSS).Learning and memory abilities were evaluated using the Morris water maze(MWM)test.Neuropathological morphological changes in the hippocampus were analyzed by hematoxylin-eosin(HE)and Nissl staining,followed by pathological scoring.Apoptosis in hippocampal tissue was detected using the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)assay,and the apoptotic rate was calculated.Levels of interleukin(IL)-6,tumor necrosis factor-α(TNF-α),IL-1β,malondialdehyde(MDA),glutathione(GSH),and superoxide dismutase(SOD)in hippocampal homogenates were detected.Protein expression levels of phosphorylated extracellular signal-regulated kinase 1/2(p-ERK1/2)and peroxisome proliferator-activated receptor γ(PPARγ)in hippocampal tissue were detected by Western blot.Results In the model group,the hippocampal tissue showed disorganized arrangement,extensive inflammatory cell infiltration,and significant loss of Nissl bodies.Compared with those in the model group,the dexmedetomidine group and the medium-and high-dose propofol groups exhibited progressively more orderly hippocampal tissue arrangement,reduced inflammatory cell infiltration,increased Nissl bodies,escape latency were significantly shortened,and mNSS score,pathological score,apoptosis rate,levels of IL-6,TNF-α,IL-1β,MDA,and p-ERK1/2 were significantly decreased(P<0.05).The number of platform crossings,levels of SOD,GSH,and PPARγ were significantly increased(P<0.05).Conclusion Propofol can reduce hippocampal neuronal apoptosis in rat model of CPB by inhibiting the ERK1/2/PPARγ signaling pathway.关键词
丙泊酚/体外循环/神经细胞凋亡/ERK1/2/PPARγ信号通路Key words
propofol/cardiopulmonary bypass/neuronal apoptosis/ERK1/2/PPARγ signaling pathway分类
医药卫生引用本文复制引用
王飞,刘硕,王存斌..丙泊酚抑制体外循环模型大鼠神经细胞凋亡机制研究[J].中国药业,2026,35(8):64-70,7.基金项目
天津市卫生健康科技项目[TJWJ2022MS752]. （）
