文献类型：期刊文献

英文题名：Ionized Angelica polysaccharides derivatives slow tumor growth in vivo and induce the apoptosis of HepG2 cells via mitochondria death receptor-mediated pathways in vitro

作者：Yang, Yanmei[1];Wang, Jie[2];Zhang, Yan[2];Xue, Weijiao[2];Chen, Yongfang[1];Yue, Jiayu[1];Wen, Yanqiao[1];Feng, Ruofei[1];Tan, Chunxia[2]

第一作者：Yang, Yanmei

通信作者：Feng, RF[1];Tan, CX[2]

机构：[1]Northwest Minzu Univ, Biomed Res Ctr, Key Lab Biotechnol & Bioengn, State Ethn Affairs Commiss, Lanzhou 730030, Peoples R China;[2]Gansu Univ Chinese Med, Lanzhou 730030, Peoples R China

第一机构：Northwest Minzu Univ, Biomed Res Ctr, Key Lab Biotechnol & Bioengn, State Ethn Affairs Commiss, Lanzhou 730030, Peoples R China

通信机构：[1]corresponding author), Northwest Minzu Univ, Biomed Res Ctr, Key Lab Biotechnol & Bioengn, State Ethn Affairs Commiss, Lanzhou 730030, Peoples R China;[2]corresponding author), Gansu Univ Chinese Med, Lanzhou 730030, Peoples R China.|[10735]甘肃中医药大学;

年份：2025

卷号：315

外文期刊名：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES

收录：;EI(收录号：20252118463293);Scopus(收录号：2-s2.0-105005491564);WOS:【SCI-EXPANDED(收录号:WOS:001501927000008)】；

基金：This work was supported by Open Funds of the Biomedical Research Center from Northwest Minzu University (BRC-KF202303), Fundamental Research Funds for the Central Universities (31920240105) , Project of Administration of Tradition of Chinese Medicine of Gansu Province (GZKP-2021-35) .

语种：英文

外文关键词：Ionization polysaccharides; HepG2 cells; Huh7 cells; Apoptosis

摘要：Ionized, phosphorylated (ASP-P) and cationised (ASP-N) derivatives of Angelica sinensis polysaccharide (ASP) were evaluated for their antitumour activity. We performed the CCK-8 assay, flow cytometry, scratch healing assay and fluorescence staining assay to detect the effects of different chemical modifications of ASP on the antitumour activity of HepG2 and Huh7 cells. Western blot was performed to detect the mechanism of antitumour effect. The results showed that ASP-P and ASP-N with maximum test concentration (240 mu g center dot mL- 1) had strong inhibitory effects on HepG2 cells with inhibition rates of 52.36 % and 31.76 %, respectively. Both ASP-P and ASP-N all significantly inhibited the proliferation and migration of HepG2 and Huh7 cells. Furthermore, the study revealed that both ASP-P and ASP-N up-regulated apoptosis related proteins, such as Caspase-3, Caspase-9, cleaved-caspase 9, Apaf-1, Bid, Bax, Caspase-8, FADD, Fas and down-regulated the expression of Bcl-2 to induce apoptosis in HepG2 and Huh7 cells. This observation was further corroborated by the identification of cell-cycle arrest-associated proteins CDK4, p53 and p21, where the expression of CDK4 was down-regulated, and the expression of p53 and p21 were up-regulated. Overall, ASP-P and ASP-N inhibits proliferation and migration and induces apoptosis of HepG2 and Huh7 cells by regulating the mitochondrial apoptotic pathway to achieve antitumor activity. ASP-P and ASP-N solution was injected by subcutaneous in the nude mice bearing tumors. In comparison with the control group, ASP-P and ASP-N were found to retard tumor growth to a significant extent without exerting any influence on the body weights of mice. The ASP-N group demonstrated the most favorable outcomes, exhibiting the lowest tumor volume.