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体外培养PC12细胞,采用20μmol/Lβ淀粉样蛋白25-35(Aβ25-35)作用24h诱导细胞损伤,建立阿尔茨海默病(AD)细胞模型,研究琐琐葡萄多糖(VTP)对PC12细胞损伤的神经保护作用。设立对照组、模型组和VTP保护组(20,40,80μg/mL),CCK-8法检测各组细胞的存活率,乳酸脱氢酶(LDH)法检测细胞膜通透性及完整性,化学比色法测定细胞内超氧化物歧化酶(SOD)、丙二醛(MDA)含量,流式细胞术检测细胞凋亡率。结果显示,20,40,80μg/mLVTP可提高PC12细胞存活率,减少LDH渗漏,增加SOD活力,减少MDA含量,降低细胞凋亡率,与模型组比较有显著差异(P<0.01)。由此推论,VTP对Aβ25-35诱导的PC12细胞凋亡和氧化损伤具有明显的保护作用。
PC12 cells were cultured in vitro. Cell injury was induced by 20 μmol / L β-amyloid 25-35 (Aβ25-35) for 24 h. Cell model of Alzheimer’s disease (AD) was established to investigate the effect of VTP on PC12 cell injury The neuroprotective effect. The control group, model group and VTP protection group (20, 40, and 80μg / mL) were established. The survival rate of each group was detected by CCK-8 method. The permeability and integrity of cell membrane were detected by LDH. The contents of intracellular superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by colorimetric method. The apoptosis rate was detected by flow cytometry. The results showed that 20, 40, 80μg / mL VTP could increase the survival rate of PC12 cells, decrease the leakage of LDH, increase the activity of SOD, decrease the content of MDA and decrease the apoptosis rate of PC12 cells (P <0.01). In conclusion, VTP has a significant protective effect on Aβ25-35-induced PC12 cell apoptosis and oxidative damage.