关键词: 脑胶质瘤, 硫氯双酚, 凋亡, JNK信号通路

Abstract: Objective To observe the anti-tumor activity of anti-parasite drug Bithionol and investigate the possible mechanism. Methods The viability of glioma cells was measured by CCK8 assay. The cell apoptosis was assayed by flow cytometry and Hoechst33258. Apoptosis-related proteinexpressions of Caspase 3/Cleaved caspase 3,PARP/Cleaved PARP were determined by Western blotting. The level of JNK-P-JNK induced by Bithionol was measuredby Western blotting with or without the treatment of JNK specific inhibitor SP600125.Results After treatment of Bithionol for 24 hours,the growth of glioma cell U251,U87were significantly inhibited in dose-dependent manner(P<0.05); and Bithionol increased U251 cell apoptosis alsoin dose-dependent manner (P< 0. 05). Compared with the control group, the levels of Caspase 3/Cleaved caspase 3,PARP/Cleaved PARPwere significantlyincreased in Bithinol treatment group(P<0. 05). JNK was activated in the U251 cells exposed to Bithinol and the phosphorylation of JNKalso increased. This activation of apoptosis could be reversed by the pre-treatment of SP600125. Conclusion Bithinol may induceapoptosis in glioma cell and the mechanism may be related to the activation of JNK-P-JNK signaling pathway.

Key words: glioma cell, Bithionol, Apoptosis, JNK signaling pathway