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目的探讨参麦注射剂对H_2O_2诱导PC12细胞氧化损伤的保护作用,并初步探讨其保护机制。方法分别向各给药组加入终浓度2.5、5、10 m L·L-1参麦注射剂,孵育0.5 h后,以H_2O_2(100μmol·L-1)刺激PC12细胞1 h造成的细胞氧化应激损伤模型。之后测定细胞存活率、乳酸脱氢酶(LDH)泄漏率、丙二醛(MDA)生成量和超氧化物歧化酶(SOD)活力,并采用Western blot法测定MAPK信号通路的变化。结果参麦注射剂能明显提高H_2O_2氧化损伤PC12模型细胞的存活率(P<0.01);参麦注射剂(2.5、5、10 m L·L-1)降低模型细胞LDH泄漏率(P<0.01),抑制MDA生成,增加SOD活力(P<0.01)。参麦注射剂可降低由H_2O_2刺激引起的Caspase-3上调,以及MAPK通路上的IKKβ、p38、ERK1的上调,通过MAPK通路保护损伤的PC12细胞。结论参麦注射剂在体外拟神经元工具细胞—PC12细胞上具有抗氧化损伤的作用。
Objective To investigate the protective effect of Shenmai injection on H 2 O 2 -induced oxidative damage in PC12 cells and to explore its protective mechanism. Methods Smectite injection (2.5, 5, 10 m L · L -1) was added to each group at different concentrations. After incubated for 0.5 h, the oxidative stress of PC12 cells induced by H 2 O 2 (100 μmol·L -1) Damage model. Cell viability, lactate dehydrogenase (LDH) leakage rate, malonyldialdehyde (MDA) production and superoxide dismutase (SOD) activity were measured. The changes of MAPK signal pathway were determined by Western blot. Results Shenmai injection significantly increased the survival rate of PC12 cells exposed to H 2 O 2 (P <0.01). Shenmai injection (2.5, 5 and 10 m L·L -1) reduced the LDH leakage rate of model cells (P <0.01) Inhibit the formation of MDA and increase the activity of SOD (P <0.01). Shenmai injection can reduce the upregulation of Caspase-3 induced by H 2 O 2 stimulation and the up-regulation of IKKβ, p38 and ERK1 in MAPK pathway and protect the injured PC12 cells through MAPK pathway. Conclusion Shenmai injection has the anti-oxidative effect on the in vitro neuronal cell-PC12 cells.