文献类型：期刊文献

英文题名：Astragalus polysaccharide protects formaldehyde-induced toxicity by promoting NER pathway in bone marrow mesenchymal stem cells

作者：She, Yali[1,2];Zhao, Xiaowen[1];Wu, Pingfan[1];Xue, Ling[1];Liu, Zhe[1];Zhu, Meng[1];Yang, Jie[1];Li, Yaling[1,2]

第一作者：舍雅莉

通信作者：Li, YL[1]

机构：[1]Gansu Univ Chinese Med, Sch Basic Med, Dept Pathol, Lanzhou, Gansu, Peoples R China;[2]Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Study Prev, Lanzhou, Gansu, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Study Prev, Lanzhou, Gansu, Peoples R China.|[10735]甘肃中医药大学;

年份：2021

卷号：59

期号：2

起止页码：124

外文期刊名：FOLIA HISTOCHEMICA ET CYTOBIOLOGICA

收录：;Scopus(收录号：2-s2.0-85110594242);WOS:【SCI-EXPANDED(收录号:WOS:000670634700006)】；

基金：1 This study was supported by the National Natural Science Foundation of China (grant number 81560667), the National Natural Science Foundation of Gansu Province, China (grant number 1506RJZA045), the Provincial-Level Key Laboratory of Molecular Medicine of Major Diseases and Study on Prevention and Treatment of Traditional Chinese Medicine, Gansu University of Chinese Medicine, China (grant number FZYX17-18-7) and Longyuan Youth Innovation and Entrepreneurship Talent Project, Gansu University of Chinese Medicine, China (grant number LYQN2021-2).

语种：英文

外文关键词：astragalus polysaccharide; formaldehyde; bone marrow mesenchymal stem cells; toxicity; NER pathway; DNA strand breakage; DNA-protein crosslinks; micronucleus formation

摘要：Introduction. In our previous study, it has been confirmed that formaldehyde (FA) not only inhibits the proliferative activity, but also causes DNA-protein crosslinks (DPCs) formation in bone marrow mesenchymal stem cells (BMSCs). The purpose of this study was to detect the protective effect of astragalus polysaccharide (APS) against the cytotoxicity and genotoxicity of BMSCs exposed to FA, and to explore potential molecular mechanisms of APS activity. Material and methods. Human BMSCs were cultured in vitro and randomly divided into control cells (Ctrl group), FA-treated cells (FA group, 120 mu mol/L), and cells incubated with FA and increasing concentrations (40, 100, or 400 mu g/mL) of APS (FA + APS groups). Cytotoxicity was measured by MTT assay. DNA strand breakage, DNA-protein crosslinks (DPCs), and micronucleus formation were respectively detected by comet assay, KCl-SDS precipitation assay, and micronucleus assay. The mRNA and protein expression level of xeroderma pigmentosum group A (XPA), xeroderma pigmentosum group C (XPC), excision repair cross-complementation group 1 (ERCC1), replication protein A1 (RPA1), and replication protein A2 (RPA2) were all detected by qRT-PCR and Western Blot. Results. Compared with the FA group, the cytotoxicity, DNA strand breakage, DPCs, and micronucleus levels were decreased significantly in FA + APS groups (P < 0.01). Meanwhile, the mRNA and protein expression of XPA, XPC, ERCC1, RPA1, and RPA2 were up-regulated significantly in the FA + APS groups (P < 0.05) with the most prominent effect of the 100 mu g/mL APS. Conclusions. Our results suggest that APS can protect the cytotoxicity and genotoxicity of human BMSCs induced by FA. The mechanism may be associated with up-regulated expression of XPA, XPC, ERCC1, RPA1, and RPA2 in the nucleotide excision repair (NER) pathway which promotes DNA damage repair.