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Autophagy is a major mechanism for the dual effects of curcumin on renal cell carcinoma cells

机译:自噬是姜黄素对肾细胞癌细胞进行双重影响的主要机制

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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 mu M and no significant change at 20 mu M but a decrease at 80 mu M. 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 mu M and 20 mu M of curcumin were significantly decreased; however, when treated with the inhibitor of the oxidative stress pathway, the LC3II levels of RCC cells at 80 mu M 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.
机译:本研究的目的是探讨姜黄素对肾细胞癌(RCC)的影响通过调节自噬。在用不同浓度的姜黄素处理后,通过RCC细胞中的MTT测定法测定细胞活性。建立ATG7沉默的RCC细胞以测试自噬作用。通过Western印迹分析了自噬途径上的关键蛋白水平。我们发现,在24小时姜黄素处理后,RCC细胞的可行性在5μm的5μm增加,并且在20 mu m下没有显着变化,但在80 mu m下降。这些效果受到抑制的抑制作用。当与AMPK和ER应激途径的抑制剂预孵育时,5μm和20μm姜黄素的RCC细胞的LC3II水平显着降低;然而,当用氧化应激途径的抑制剂处理时,80μm在80μm的LC3II水平显着降低。总之,本研究表明姜黄素受保护的细胞在低浓度下死亡,但在高浓度下促进细胞死亡。自噬在姜黄素对RCC的影响中发挥了双重作用。 AMPK和ER应激途径可能涉及低浓度的姜黄素以保护细胞,而氧化应激途径可能在高姜黄素浓度下参与毒性。

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