Chaperones are the target in aloe-emodin-induced human lung nonsmall carcinoma H460 cell apoptosis.

摘要: Abstract Our previous study has demonstrated that aloe-emodin induced a significant change in the expression of apoptosis-related proteins H460 cells. However, molecular mechanisms underlying biological effects still remain unknown. The present applied 2D electrophoresis (pH range 4–7) to involved (40 μM)-induced cell apoptosis. Eleven were found markedly change. These altered identified as ATP synthase, vimentin, HSP60, HSP70 and protein disulfide isomerase. Aloe-emodin caused time-dependent decrease intracellular levels, which might be related direct inhibition synthase. We also observed activity mitochondria was injured by aloe-emodin. data clearly may play critical role aloe-emodin-induced death. Many reports emphasize chaperones have complex suggested increasing HSP70, 150 kDa oxygen-regulated isomerase is are endoplasmic reticulum chaperone. Therefore, we hypothesized stress serves promote apoptosis after treatment with death through caspase-3 apoptotic pathway, but not apoptosis-inducing factor pathway.