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Self-Protection against Triptolide-Induced Toxicity in human hepatic cells via Nrf2-ARE-NQO1 Pathway

Chinese Journal of Integrative Medicine 2017年第12期23卷 929-936页

作者： ZHOU Ling-ling ZHOU Cong LIANG Xiao-wen FENG Zhe LIU Zhang-pu WANG Hao-lu ZHOU Xue-ping School of Pharmacy The First Clinical Medical CollegeNanjing University of Chinese MedicineNanjing 210023China Department of Pharmacy Wuxi No.9 People's HospitalSoochow UniversityWuxi Hand Surgery HospitalWuxiJiangsu Province 214062China Therapeutics Research Centre School of MedicineThe University of QueenslandPrincess Alexandra HospitalWoolloongabba QLD 4102Australia

Objective: To find the signaling pathway of triptolide(TP)-induced liver injury and to reveal whether NF-E2-related factor 2(Nrf2) plays an important role in cellular self-protection. Methods: The L-02 and HepG2 cells were cultured and treated with various concentrations of TP. The cell viability was observed, and the cell medium was collected for detecting the aspartate aminotransferase(ALT), alanine aminotransferase(AST), lactate dehydrogenase(LDH), superoxide dismutase(SOD) and L-glutathione production(GSH) levels. Nrf2 and its downstream target NAD(P)H: quinine oxidoreductase 1(NQO1) and heme oxygenase-1(HO-1) expression, the nuclear translocation of Nrf2, and the binding ability of Nrf2 and antioxidant response element(ARE) were also identified. Meanwhile,shRNA was used to silence Nrf2 in L-02 cells to find out whether Nrf2 plays a protective role. Results: The viability of the L-02 and HepG2 cells treated with TP decreased in a doseand time-dependent manner, and TP(20–80 μg/mL) markedly induced the release of ALT, AST and LDH(Pcells(Phuman hepatic cells treated with TP induced oxidative stress, and led to cytotoxicity. Self-protection against TP-induced toxicity in human hepatic cells might be via Nrf2-ARE-NQO1 transcriptional pathway.

关键词： triptolide human hepatic cells NF-E2-related factor 2 oxidative stress liver injury

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