Fig. 6. LCH increases mitochondrial membrane potential (MMP) dysfunction in HCT116 and HCT116-OxR CRC cells. (A) Cells were treated with or without 4, 8 and 12 µM of LCH for 48 h, and then MMP depolarization was determined using flow cytometric analysis after staining with a Muse® MitoPotential kit. (B) The histogram of total MMP depolarized cells (%). Results are presented as mean ± SD (*p<0.05, **p<0.01, and ***p<0.001 compared to the control group). (C) The expression of ER stress (GRP78, CHOP, DR4, and DR5), mitochondria-mediated apoptosis (Bim and Bax) and antiapoptosis (Mcl-1, Bcl-xL, and Bcl-2) proteins was examined by Western blotting. And the expression of apoptosis-associated proteins was examined. For determining the cyto c levels, cytosol and mitochondrial fraction proteins were separated, and α-Tubulin and COX4 were used as cytosolic and mitochondrial controls, respectively. Actin was used as an internal control for equal loading.
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