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PO1-9-13

Bushen-Jianpi dedoction prolong survival of hepatocellular carcinoma patients involved in apoptosis induction of hepatoma cells by regulating PI3K-Akt-mTOR signal pathway

[Speaker] Shi-Bing Su:1
[Co-author] Rong Wu:1, Xiao-Yan Li:1, Fei-Fei Cai:1, Meng-Die Yang:1
1:Research Center for Traditional Chinese Medicine Complexity System, Shanghai University of Traditional Chinese Medicine, China

This study was conducted to investigate the effective mechanisms of Bushen-Jianpi (BSJPD) decoction in hepatocellular carcinoma (HCC) by clinical therapy data, network pharmacology analysis and In Vitro pharmacological experimental verification. The univariate and cox regression analysis revealed that BSJPD was protective factor (P<0.05). The median survival time of BSJPD group (11 months) was longer than that in control group (8 months) (P<0.05). Network pharmacology analysis showed that there are 143 compounds, 56 targets and 10 pathways in BSJPD, among 9 compounds including quercetin, kaempferol, beta-sitosterol, stigmasterol, hederagenin, formononetin, naringenin, isorhamnetin, licochalcone A and alisol B are important network node. Drug serum with 20% BSJPD inhibited the cell viability (p<0.05), induced the cell apoptosis (p<0.01) and reduced the levels of PI3K, P-Akt and BCLXL expressions, increased the p53 and Cleaved CASP9 and Cleaved CASP3 expressions (p<0.05) in HepG2 cells. Moreover, Licochalcone A, alisol B and hederagenin inhibited the cells viability (p<0.05), induced the cell apoptosis (p<0.01) and reduced P-Akt expressions, improved the levels of p53 and Cleaved CASP3 (p<0.05) in HepG2 cells. It suggested that BSJPD prolong survival of HCC patients may involve in apoptosis induction of hepatoma cells by regulating PI3K-Akt-mTOR signal pathway and p53, CASP3, 9 and BCLXL/BAD.
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