作者: Mengtao Zhou , Yukai Xiang , Wen Ye , Chaohao Huang , Bin Lou
DOI: 10.1016/J.BBRC.2017.04.133
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摘要: Brusatol, isolated from brucea, has been proved to exhibit anticancer influence on various kind of human malignancies. However, the role that brusatol plays in pancreatic cancer is seldom known by public. Through researches was inhibit growth and induce apoptosis both PATU-8988 PANC-1 cells decreasing expression level Bcl-2 increasing levels Bax, Cleaved Caspase-3. Then we found activation JNK, p38 MAPK inactivation NF-κb, Stat3 are related with potential pro-apoptotic signaling pathways. SP600125 could not only abrogated JNK caused brusatol, but also reverse decrease as SB203580 did. Besides, reversed NF-κb Stat3. Furthermore, BAY 11–7082 S3I-201 indeed had similar effect Phospho-Stat3 Bcl-2. To sum up, came a conclusion cancer, do apoptosis. And inferred illustrates attribution via JNK/p38 MAPK/NF-κb/Stat3/Bcl-2 pathway.