Secalonic acid A reduced colchicine cytotoxicity through suppression of JNK, p38 MAPKs and calcium influx

作者：Zhai, Aifeng; Zhang, Yi; Zhu, Xiaonan; Liang, Jinting; Wang, Xuelan; Lin, Yongcheng^*; Chen, Ruzhu

来源：Neurochemistry International, 2011, 58(1): 85-91.

DOI：10.1016/j.neuint.2010.10.016

• Secalonic acid A
• Neuronal apoptosis
• Colchicine
• JNK
• Calcium
• Caspase-3

There are few articles about the cytotoxicity evoked by secalonic acid A (SAA) in some tumor cells. It has not yet been reported whether SAA has any action on neurons of the central nervous system. The aim of this study was to investigate the protective effect of SAA against apoptosis of rat cortical neurons induced by colchicine. The protective action of SAA on the cortical neurons treated with colchicine at 1 mu M was examined by Hoechst 33258, LDH release and flow cytometry methods. The results from the above tests indicated that SAA at 3 and 10 mu M significantly prevented colchicine-induced apoptosis of the cortical neurons. Further studies from Western blot and confocal microscopy experiments showed that the activation of JNK, p38 MAPKs and caspase-3 during neuron apoptosis triggered by 1 mu M colchicine could be obviously suppressed by SAA; on the other hand, an increase in the intracellular free Ca2 by 1 mu M colchicine in the cortical neuron was blocked evidently by SAA. The above results suggested that SAA could antagonize the cytotoxicity of colchicine in the rat cortical neurons, which may be through inhibition of phosphorylation of JNK and p38 MAPKs, calcium influx, and the activation of caspase-3.

• 出版日期2011-1
• 单位中山大学