Colchicine-induced apoptosis in human normal liver L-02 cells by mitochondrial mediated pathways

Colchicine is an alkaloid that has been widely used to treat gout. It also has a curative effect on cancer. Although many studies have shown that its effect on cell apoptosis was mediated by the activation of caspase-3, the pathways involved in the process remained obscure. Here we show some evidence regarding the missing information using human normal liver cells L-02 in our study. The effect of colchicine on apoptosis in L-02 cells and the apoptosis-associated signaling pathways were determined using different tests including cell viability assay, Annexin V and propidium idodide binding, PI staining, Hoechst 33342 staining, mitochondrial membrane potential assay, caspase activity assay and Western blot analysis. We found that colchicine-induced a dose-dependent drop of cell viability in L-02 cells; early apoptosis happened when cells were treated with 0.1 μM of colchicine. The colchicine-induced loss of mitochondrial membrane potential, activation of caspase-3 and 9, up-regulation of Bax and down-regulation of Bcl-2 showed an evidence for the colchicine activity on apoptosis, at least, by acting via the intrinsic apoptotic pathway.

► We found colchicine-induced a dose-dependent drop of cell viability in L-02 cells.
► Colchicine could up-regulate Bax, down-regulate Bcl-2 and activate caspase-3 and 9.
► AST and ALT were unfit as test items for the hepatic damage of the L-02 cells.
► Colchicine could induce apoptosis in L-02 cells through the mitochondrial pathway.