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目的研究异丙酚对肿瘤坏死因子-α(TNF-α)诱导小鼠脊髓神经元凋亡的影响。方法脊髓神经元取自孕14 d胎龄小鼠的胎鼠,于含B27的神经细胞培养基中培养7 d后,随机分为6组:对照组(Con组);50μmol／L异丙酚组(P50组);TNF-α组(TNF-α组);25μmol／L异丙酚+TNF-α组(P25+ TNF-α组);50μmol／L异丙酚+TNF-α组(P50+TNF-α组);100μmol／L异丙酚+TNF-α组(P100+TNF-α组),各组中加入相应终浓度的异丙酚孵育30 min,再加入TNF-α至终末浓度为2 000 U／ml,培养24 h后,采用碘化丙锭／Hoechst 33342双染法检测细胞凋亡,计算细胞凋亡率,采用免疫细胞化学方法测定Bcl-2表达。结果与Con组比较,TNF-α组神经元凋亡率升高,Bcl-2表达降低(P<0．01),不同浓度异丙酚预先给药可减弱TNF-α诱导的上述改变(P<0．05)。结论异丙酚可抑制TNF-α诱导小鼠脊髓神经元的凋亡,其机制与上调Bcl-2表达有关。
Objective To investigate the effect of propofol on the apoptosis of spinal cord neurons induced by tumor necrosis factor-α (TNF-α) in mice. Methods Spinal cord neurons were fetched from 14-day-old pregnant mice and cultured in B27-containing neural cell culture medium for 7 days. They were randomly divided into 6 groups: control group (Con group), 50μmol / L propofol (P50 group); TNF-α group (TNF-α group); 25μmol / L propofol + TNF-α group (P25 + TNF-α group); 50μmol / L propofol + TNF- TNF-α group); 100μmol / L propofol + TNF-α group (P100 + TNF-α group), the same concentration of propofol was added to each group for 30 min, then TNF- 2 000 U / ml. After cultured for 24 h, the apoptosis rate was detected by propidium iodide / Hoechst 33342 double staining and the apoptosis rate was calculated. The expression of Bcl-2 was detected by immunocytochemistry. Results Compared with Con group, the apoptotic rate of TNF-α group was increased and the expression of Bcl-2 was decreased (P <0.01). Preconditioning with different concentrations of propofol attenuated the above changes induced by TNF-α (P <0.05). Conclusion Propofol can inhibit the TNF-α-induced apoptosis of spinal cord neurons in mice, and its mechanism is related to the up-regulation of Bcl-2 expression.