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Epigallocatechin Gallate Induces Acute Promyelocytic Leukemia NB4 Cells Apoptosis by Activation of p38α
Gan Liugen1,2, Liu Beizhong1,2, Shan Zhiling2, Xiao Chunlan1,2, Xu Ting1,2, Song Hao1,2, Li Liu2, Yang Rong2, Zhong Liang2*
1Central Laboratory, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China;
2Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Faculty of Laboratory Medical, Chongqing Medical University, Chongqing 400016, China
2Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Faculty of Laboratory Medical, Chongqing Medical University, Chongqing 400016, China
Abstract: This study was aimed to investigate the molecular mechanism of NB4 cells apoptosis induced by epigallocatechin gallate (EGCG). NB4 cells were treated with EGCG in a dose-dependent manner. Or NB4 cells were pretreated with PD169316， an inhibitor of p38α， then treated with EGCG. The proliferation of NB4 cells was detected by cell counting kit-8 (CCK-8) assay. The apoptosis of NB4 cells was measured by FITC-AnnexinV/PI. The protein levels of p38α， P-p38α， Bcl-2 and Bax were detected by Western blot. The results indicated that EGCG treatment significantly inhibited the viability of NB4 cells in a dose-dependent manner. In addition， EGCG treatment induced apoptosis， increased Bax and P-p38α protein expression levels and decreased Bcl-2 protein expression levels. Pretreatment with PD169316 partially increased the viability of NB4 cells， meanwhile， blocked EGCG-induced apoptosis and inhibited EGCG-mediated increases in Bax expression， but not affected Bcl-2 expression. These results suggested that EGCG induced apoptosis in NB4 cells may through the activation of p38α.
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