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目的:应用过氧化氢(H2O2)孵育原代大鼠皮层细胞制作细胞损伤模型,研究大黄素对模型细胞凋亡的影响。方法:H2O2和大黄素对皮层细胞进行处理,MTT和LDH法检测细胞活性,流式细胞术检测细胞内活性氧(ROS)水平,倒置显微镜、Hoechst33258染色观察细胞形态变化,Western blot法检测Bcl-2和Bax的表达。结果:与正常对照组比较,经150μmol/LH2O2处理后皮层细胞活性显著降低,ROS聚集增加,Hoechst33258荧光染色出现明亮的凋亡小体,大黄素预处理能改善其损害情况。Western blot法显示与正常对照组比较,H2O2可致Bcl-2表达显著减弱,Bax表达显著增强,而大黄素预处理可使其恢复到正常水平。结论:大黄素可拮抗过氧化氢诱导的皮层神经细胞凋亡,具有一定的神经细胞保护功能。
OBJECTIVE: To establish a cell injury model by using hydrogen peroxide (H2O2) to incubate primary rat cortical cells to study the effect of emodin on apoptosis of model cells. METHODS: Cortical cells were treated with H2O2 and emodin. Cell viability was measured by MTT assay and LDH assay. ROS levels were measured by flow cytometry. Cell morphology was observed by Hoechst33258 staining. Bcl- 2 and Bax expression. Results: Compared with the normal control group, the cortical cell activity was significantly decreased and the ROS accumulation was increased after treated with 150μmol / LH 2 O 2. Bright apoptotic bodies were observed by Hoechst 33258 staining. Emodin pretreatment could improve the damage of cortical cells. Western blot showed that compared with the normal control group, H2O2 induced a significant decrease of Bcl-2 expression and a significant increase of Bax expression, while emodin pretreatment returned to normal levels. Conclusion: Emodin can antagonize hydrogen peroxide-induced apoptosis of cortical neurons and has certain neuroprotective function.