斯钙素2在舒芬太尼联合丙泊酚麻醉过程中诱导神经细胞凋亡的作用研究

Role of STC2 in sufentanil combined with propofol induced neuronal apoptosis during anesthesia

目的:探讨斯钙素2(STC2)对舒芬太尼联合丙泊酚(SF+PP)诱导的神经细胞凋亡的影响及其分子机制。方法:使用1 mmol/L舒芬太尼联合不同浓度梯度的丙泊酚(0.2、0.4、0.8、1.6、3.2 mmol/L)处理SH-SY5Y细胞24 h,CCK-8检测细胞活力,初步确定SF+PP的细胞毒性作用;使用1 nmol/L舒芬太尼联合低中高剂量丙泊酚(0.2、0.4、0.8 mol/L)处理SH-SY5Y细胞24 h,TUNEL染色检测各组细胞凋亡情况、qRT-PCR和Western blot法检测STC2,及磷脂酰肌醇3激酶/蛋白激酶B(PI3K/AKT)信号通路的mRNA和蛋白表达水平。结果:SF+PP处理显著抑制了人神经母细胞瘤细胞(SH-SY5Y)细胞活力,在选取的低、中、高剂量SF+PP处理后细胞凋亡增加(P<0.05),SF+PP干预后SH-SY5Y细胞内STC2,磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(AKT)的mRNA和蛋白表达水平显著升高(均P<0.05)。结论:STC2参与舒芬太尼联合丙泊酚在麻醉过程中诱导的神经细胞凋亡,其机制与STC2激活PI3K/AKT信号通路相关。

Objective:To investigate the effect of stannocalcin 2(STC2)on nerve cell apoptosis induced by sufentani combined with propofol(SF+PP)and its molecular mechanism.Methods:SH-SY5Y cells were treated with 1 mmol/L sufentanil combined with propofol with different concentration gradients(0.2,0.4,0.8,1.6,3.2 mmol/L)for 24 hours,and the cytotoxicity of SF+PP was preliminarily determined by CCK-8.SH-SY5Y cells were treated with 1 mmol/L sufentanil combined with high-,medium-and low-dose of propofol(0.2,0.4,0.8 mmol/L)for 24 hours,and apoptosis was detected by TUNEL staining,and the mRNA and protein expression levels of STC2 and PI3K/AKT signaling pathway were detected by qRT-PCR and Western blot.Results:SF+PP treatment significantly inhibited the viability of SH-SY5Y cells,and the apoptosis increased after treatment by the low-,medium-and high-dose of SF+PP(all P<0.05).After SF+PP intervention,the mRNA and protein expression levels of STC2,PI3K and AKT in SH-SY5Y cells were increased significantly(all P<0.05).Conclusion:STC2 is involved in sufentanil-propofol-induced neuronal apoptosis,which is related to the activation of PI3K/AKT signaling pathway by STC2.