文献类型：期刊文献

英文题名：Combination of chloroquine diphosphate and salidroside induces human liver cell apoptosis via regulation of mitochondrial dysfunction and autophagy

作者：Jiang, Bing[1];Feng, Longfei[1];Yang, Tao[1];Guo, Wenjing[1];Li, Yangyang[1];Wang, Tao[2];Liu, Chengguang[3];Su, Haixiang[1,2,4]

第一作者：Jiang, Bing

通信作者：Su, HX[1]

机构：[1]Gansu Univ Tradit Chinese Med, Sch Basic Med, Lanzhou 730000, Gansu, Peoples R China;[2]Gansu Prov Canc Hosp, Gansu Prov Acad Inst Med Res, Translat Med Res Ctr, Lanzhou 730050, Gansu, Peoples R China;[3]Guangxi Univ Tradit Chinese Med, Clin Coll Integrated Chinese & Western Med, Nanning 530200, Guangxi, Peoples R China;[4]Gansu Prov Canc Hosp, Gansu Prov Acad Inst Med Res, Translat Med Res Ctr, 2 Xiaoxihu East St, Lanzhou 730050, Gansu, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Prov Canc Hosp, Gansu Prov Acad Inst Med Res, Translat Med Res Ctr, 2 Xiaoxihu East St, Lanzhou 730050, Gansu, Peoples R China.

年份：2023

卷号：27

期号：2

外文期刊名：MOLECULAR MEDICINE REPORTS

收录：;Scopus(收录号：2-s2.0-85145084632);WOS:【SCI-EXPANDED(收录号:WOS:000909537900001)】；

语种：英文

外文关键词：salidroside; chloroquine diphosphate; liver cancer; apoptosis; autophagy; PI3K; Akt; mTOR

摘要：Hepatocellular carcinoma (HCC) is the leading cause of cancer-associated death in the world. Chemotherapy remains the primary treatment method for HCC. Despite advances in chemotherapy and modalities, recurrence and resistance limit therapeutic success. Salidroside (Sal), a bioactive component extracted from the rhizome of Rhodiola rosea L, exhibits a spectrum of biological activities including antitumor effects. In the present study, it was demonstrated that Sal could induce apoptosis and autophagy of 97H cells by using CCK-8 assay, transmission electron microscopy (TEM), Hoechst33342 staining, MDC staining, western blotting. Pretreatment with Sal enhanced apoptosis and autophagy via upregulation of expression levels of Bax, Caspase-3, Caspase-9, light chain (LC)3-II and Beclin-1 proteins and downregulation of expression levels of Bcl-2, LC3-I and p62 protein in 97H cells. Furthermore, Sal was demonstrated to inhibit activation of the PI3K/Akt/mTOR signaling pathway and, when combined with autophagy inhibitor chloroquine diphosphate (CQ), increased phosphorylation of PI3K, Akt and mTOR proteins. The combined treatment with Sal and CQ not only decreased Sal-induced autophagy, but also accelerated Sal-induced apoptosis. Therefore, Sal-induced autophagy might serve a role as a defense mechanism in human liver cancer cells and its inhibition may be a promising strategy for the adjuvant chemotherapy of liver cancer.