姜黄素
自噬
活力测定
氧化应激
化学
安普克
MTT法
程序性细胞死亡
免疫印迹
细胞
药理学
细胞生物学
癌症研究
生物
生物化学
细胞凋亡
酶
蛋白激酶A
基因
作者
Qian Deng,Liang Liang,Liu Quan-hai,Wanxing Duan,Yazhuo Jiang,Liandong Zhang
标识
DOI:10.1016/j.ejphar.2018.02.038
摘要
The aim of this study was to explore the effects of curcumin on renal cell carcinoma(RCC) through regulating autophagy. Cell viabilities were determined by MTT assay in RCC cells after treatment with curcumin at different concentrations for various durations. ATG7 silencing RCC cells were established to test the role of autophagy. The levels of key proteins on autophagy pathway were analyzed by Western blot. We found out that following 24 h curcumin treatment, the viability of RCC cells had an increase at 5 μM and no significant change at 20 μM but a decrease at 80 μM. These effects were affected by the inhibition of autophagy. When pre-incubated with inhibitors of the AMPK and ER stress pathways, the LC3II levels of RCC cells at 5 μM and 20 μM of curcumin were significantly decreased; however, when treated with the inhibitor of the oxidative stress pathway, the LC3II levels of RCC cells at 80 μM were significantly decreased. In conclusion, the present study indicated Curcumin protected cells from death at low concentration but promotes cell death at high concentration. Autophagy played a dual role in curcumin's effects on RCC. The AMPK and ER stress pathways might be involved at low concentrations of curcumin to protect cells, while the oxidative stress pathway might take part in toxicity at high curcumin concentration.
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