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目的:探讨竹节参总皂苷对H2O2致SH-SY5Y细胞氧化应激损伤的保护作用及其分子机制。方法:H2O2作用SH-SY5Y细胞建立氧化应激损伤模型,以不同浓度竹节参总皂苷(0.1、1、5、20μg/m L)预处理12 h,再加入H2O2继续培养12 h。通过MTT检测细胞活力;酶生化法检测超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量;Western blotting检测Nrf2、p-ERK、p-P38蛋白表达;Real-Time PCR检测NQO1、GCLC的mRNA表达。结果:各浓度竹节参均能显著提高H2O2所导致的细胞活力降低、提高SOD活性、降低MDA含量,并能上调Nrf2、p-ERK蛋白及NQO1、GCLC mRNA表达。结论:竹节参总皂苷对H2O2致SH-SY5Y细胞氧化应激损伤具有保护作用,其作用机制可能与调控ERK/Nrf2通路,从而增强抗氧化基因表达有关。
Objective: To investigate the protective effect of SSP on oxidative stress injury induced by H2O2 in SH-SY5Y cells and its molecular mechanism. Methods: The model of oxidative stress injury was induced by H2O2 in SH-SY5Y cells. The cells were pretreated with 0.1, 1, 5, 20 μg / mL total Saponins (0.1, 1, 5 and 20 μg / mL) for 12 h. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were determined by MTT assay. The protein expressions of Nrf2, p-ERK and p-P38 were detected by Western blotting. The expressions of NQO1, GCLC mRNA expression. Results: Scutellaria barbata could significantly decrease the cell viability induced by H2O2, increase the activity of SOD, decrease the content of MDA, and upregulate the expression of Nrf2, p-ERK protein and NQO1 and GCLC mRNA. CONCLUSION: SSP can protect H2O2-induced oxidative stress injury in SH-SY5Y cells. The mechanism may be related to the regulation of ERK / Nrf2 pathway and the enhancement of anti-oxidative gene expression.