依托咪酯对过氧化氢诱导的PC12细胞损伤的影响及机制  被引量:5

Mechanism and effect of etomidate on H2O2 induced PC12 cell injury

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作  者:张建军[1] 王东[1] 尚峰 Zhang Jianjun;Wang Dong;Shang Feng(Department of Neurosurgery,the Fourth Central Hospital of Tianjin,Tianfin 300140,China;Department of Neurosurgery,Xuanwu Hospital,Capital Medical University,Beijing 100053,China)

机构地区:[1]天津市第四中心医院神经外科,300140 [2]首都医科大学宣武医院神经外科,北京100053

出  处:《中华实验外科杂志》2019年第1期100-102,共3页Chinese Journal of Experimental Surgery

基  金:天津市自然科学基金(JCYBJC18000);天津市卫生和计划生育委员会基金(2015KR20).

摘  要:目的探讨依托咪酯对过氧化氢(H2O2)诱导的PC12细胞损伤的保护作用。方法PC12细胞随机分为正常组,H2O2组(200 μmol/L H2O2),依托咪酯低、中、高浓度组,并分别检测各组细胞活力、凋亡、半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-3、Caspase-9活性、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-2(bcl-2)及bcl-2相关X蛋白(bax)蛋白表达。结果与正常组比较,H2O2组(0.38±0.03比0.65±0.06)细胞活力降低(P<0.01),细胞早期[(15.64±1.56)%比(2.32±0.23)%]及晚期凋亡率[(24.61±2.46)%比(2.09±0.21)%](P<0.01)、MDA含量(P<0.01)、Caspase-3[(4.39±0.44)比(0.58±0.05)](P<0.01)、Caspase-9[(2.95±0.29)比(0.48±0.04)]活性提高(P<0.01),SOD、CAT及GSH-Px活性降低(P<0.01),bcl-2表达量下调(P<0.01),bax表达量上调(P<0.01)。与H2O2组比较,依托咪酯低、中、高浓度组细胞活力提高(P<0.01),细胞凋亡率(P<0.01)、MDA含量(P<0.01)、Caspase-3、Caspase-9活性降低(P<0.01;P<0.01),SOD(P<0.01)、CAT(P<0.01)及GSH-Px(P<0.01)活性提高,bcl-2表达量上调(P<0.01),bax表达量下调(P<0.01)。结论依托咪酯可能通过提高抗氧化能力及抵抗细胞凋亡抑制H2O2引起的PC12细胞损伤。Objective To explore protective effect of etomidate on H2O2 induced PC12 cell injury.Methods PC12 cell was randomized into normal group, H2O2 group (200 μmol/L H2O2), etomidate low, medium and high-dose group. Cell viability, cell apoptotic rate, malondialdehyde (MDA) content, the activity of cysteinyl aspartate specific proteinase (Caspase)-3, Caspase-9, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), the expression of B-cell lymphoma-2 (bcl-2) and bcl-2 associated X protein (bax) was measured.Results Compared with normal group, cell viability [(0.38±0.03) vs. (0.65±0.06)] was decreased (P<0.01), the cell late apoptotic rate [(15.64±1.56)% vs. (2.32±0.23)%], cell late apoptotic rate [(24.61±2.46)% vs. (2.09±0.21)%], the activity of Caspase-3 [(4.39±0.44) vs. (0.58±0.05)], Caspase-9 [(2.95±0.29) vs. (0.48±0.04)], MDA content was increased (P<0.01), the activity of SOD, CAT and GSH-Px was decreased (P<0.01), the expression of bcl-2 was down-regulated (P<0.01), the expression of bax was up-regulated (P<0.01). Compared with H2O2 group, cell viability was increased (P<0.01), the cell apoptosis rate (P<0.01), the activity of Caspase-3 (P<0.01), Caspase-9 (P<0.01), MDA content was reduced (P<0.01), the activity of SOD (P<0.01), CAT (P<0.01) and GSH-Px (P<0.01) was increased, the expression of bcl-2 was up-regulated (P<0.01), the expression of bax was down-regulated (P<0.01).Conclusion Etomidate could suppress H2O2 induced PC12 cell injury via increasing antioxidant capacity and resistance to cell apoptosis.

关 键 词:依托咪酯 PC12细胞 过氧化氢 损伤 

分 类 号:R651[医药卫生—外科学]

 

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