右美托咪定对过氧化氢引起的PC12细胞损伤的保护作用

Protective effect of dexmedetomidine on PC12 cell injury induced by H_2O_2

目的探讨右美托咪定对过氧化氢(H_2O_2)引起的PC12细胞损伤的保护作用。方法 PC12细胞随机分为正常对照组,H_2O_2组(200μmol/L H_2O_2),右美托咪定低、中、高浓度组(50、100、200μmol/L右美托咪定+200μmol/L H_2O_2),培养48 h,分别检测细胞活力、凋亡情况、天冬氨酸蛋白水解酶(Caspase)3、Caspase9活性、乳酸脱氢酶(LDH)释放量,丙二醛(MDA)含量,超氧化物歧化酶(SOD)、过氧化氢酶(CAT)及谷胱甘肽过氧化物酶(GSH-Px)活性、B淋巴细胞瘤(Bcl)-2及Bcl-2相关X蛋白(Bax)蛋白表达、细胞外调节蛋白激酶(ERK)1/2磷酸化水平。结果与H_2O_2组比较,右美托咪定低、中、高浓度组细胞活力显著提高,细胞早期及晚期凋亡率显著降低,LDH释放量显著减少,MDA含量显著降低,SOD、CAT及GSH-Px活性显著升高,Caspase3、9活性显著降低,Bcl-2及p-ERK1/2表达量显著上调,Bax表达量显著下调(均P<0.01)。结论右美托咪定能通过抗氧化及抗细胞凋亡进而抑制H_2O_2引起的PC12细胞损伤。

Objective To explore protective effect of dexmedetomidine on PC12 cell injury induced by H2O2.Methods PC12 cell was randomized into normal control,H2O2（ 200 μmol/L H2O2）,dexmedetomidine low,medium and high-dose groups（ 50,100,200 μmol/L dexmedetomidine ＋200 μmol/L H2O2） and was cultured for 48 h. Cell viability,cell apoptosis,the activity of cysteinyl aspartate specific proteinase（ Caspase） 3,Caspase9,lactate dehydrogenase（ LDH） release,malondialdehyde（ MDA） content,the activity of superoxide dismutase（ SOD）,catalase（ CAT） and glutathione peroxidase（ GSH-Px）,the expression of B-cell lymphoma（ Bcl）-2,Bcl-2 associated X protein（ Bax）,phosphorylation of extracellular regulated protein kinases 1/2（ ERK1/2） were measured. Results Compared with H2O2 group,cell viability was increased（ P〈0. 01）,the cell apoptosis rate,the activity of Caspase3,Caspase9,LDH release and MDA content were reduced（ P〈0. 01）,the activity of SOD,CAT and GSH-Px were increased（ P〈0. 01）,the expression of Bcl-2 and p-ERK1/2 were up-regulated（ P〈0. 01）,the expression of Bax was down-regulated（ P〈0. 01） in dexmedetomidine low,medium and high-dose groups.Conclusions Dexmedetomidine suppresses PC12 cell injury induced by H2O2 via anti-oxidation and anti-apoptosis.