论文部分内容阅读
研究南岭柞木苷G对β淀粉样蛋白25-35片断(Aβ25-35)诱导的PC12细胞损伤的保护作用。用25 μM聚集状的Aβ25-35 建立神经细胞损伤模型,将培养的PC12细胞分为空白对照组,Aβ25-35模型组,Aβ25-35+药物组, 采用MTT比色法,Hoechst 33342染色法分析细胞存活率,流式细胞仪定量分析细胞凋亡率,以2′,7′-二氢二氯荧光黄双乙酸钠(DCFH-DA)为标记探针检测细胞内产生的活性氧含量。(1) 25 μM聚集状的Aβ25-35处理PC12细胞24 h能显著降低细胞活力,诱导细胞发生凋亡,凋亡率达34.26% 细胞内活性氧水平上升。(2) 南岭柞木苷G与聚集状的Aβ25-35共同孵育,可提高细胞存活率流式细胞仪检测凋亡率降低到22.62% 以DCFH-DA为标记探针检测,南岭柞木苷G可明显抑制聚集状的Aβ25-35引起的细胞内活性氧的产生。南岭柞木苷G能抑制Aβ25-35诱导的PC12神经细胞的凋亡,其神经细胞保护作用可能与降低细胞内活性氧水平有关。
To study the protective effect of Nanling acumin G on the injury of PC12 cells induced by β-amyloid 25-35 fragment (Aβ25-35). The nerve cell injury model was established with 25 μM aggregated Aβ25-35. The cultured PC12 cells were divided into blank control group, Aβ25-35 model group and Aβ25-35+ drug group. The MTT colorimetric method was used for Hoechst 33342 staining analysis. Cell viability was assessed by flow cytometry, and 2’,7’-dihydrodichlorofluorescein diacetate (DCFH-DA) was used as a labeled probe to detect the amount of reactive oxygen species produced in the cells. (1) PC12 cells treated with 25 μM aggregated Aβ25-35 for 24 h significantly reduced cell viability and induced apoptosis. The apoptotic rate reached 34.26% and the level of reactive oxygen species in the cells increased. (2) Nanling acumin G co-incubated with aggregated Aβ25-35 can increase cell viability. The rate of apoptosis was reduced to 22.62% by flow cytometry. DCFH-DA was used as a labeled probe for detection. Glycoside G significantly inhibited the production of reactive oxygen species in cells induced by aggregated Aβ25-35. Nanling acumin G can inhibit the apoptosis of PC12 neurons induced by Aβ25-35, and its neuroprotective effect may be related to the decrease of intracellular reactive oxygen species.