文献类型：期刊文献

英文题名：Intervention effects of sulfate glycosaminoglycan from swim bladder against arsenic-induced damage in IEC-6 cells

作者：Ou, Jieying[1];Wang, Zhuo[1];Huang, Houpei[1];Chen, Jing[1];Liu, Xiaofei[1];Jia, Xuejing[1];Song, Bingbing[1];Cheong, Kit-Leong[1];Gao, Yuan[1];Zhong, Saiyi[1,2,3]

机构：[1]Guangdong Ocean Univ, Coll Food Sci & Technol, Guangdong Prov Key Lab Aquat Prod Proc & Safety, Guangdong Prov Engn Lab Marine Biol Prod,Guangdong, Zhanjiang 524088, Peoples R China;[2]Guangdong Ocean Univ, Shenzhen Res Inst, Shenzhen 518108, Peoples R China;[3]Dalian Polytech Univ, Collaborat Innovat Ctr Seafood Deep Proc, Dalian 116034, Peoples R China

年份：2023

卷号：252

外文期刊名：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES

收录：SCI-EXPANDED(收录号：WOS:001073827200001)、、EI(收录号：20233814758847)、Scopus(收录号：2-s2.0-85171584326)、WOS

基金：This research project is supported by the grants from National Nat- ural Science Foundation of China (No: 31972163) , the National Key Research and Development Project (2019YFD0902005) , the Innovative Team Program of High Education of Guangdong Province (2021KCXTD021) and Zhanjiang Ocean Youth Talent Innovation Project (2021E05019) .

语种：英文

外文关键词：Glycosaminoglycan; Heavy metals; Intestinal epithelial cells

外文摘要：In this study, a purified macromolecular sulfate glycosaminoglycan whose structural characterization is similar to chondroitin sulfate from the swim bladder of Aristichthys nobilis, named SBSG, was used to explore the intervention effects on arsenic-induced intestinal epithelial cells (IEC-6) damage. Arsenic exposure led to cell membrane rupture, mitochondrial dysfunction, oxidative damage, and down-regulation of tight junction proteins expression. Treatment with SBSG could alleviate arsenic exposure-induced cell damage by decreasing the extracellular lactate dehydrogenase activity and influencing mitochondrial membrane potential, reactive oxygen species level, malondialdehyde content, and anti-oxidative enzyme activity. On the other hand, SBSG could promote nitric oxide production to achieve potential immunoregulation. The Western blot showed that intervention of SBSG mainly could restrain the activation of the JNK signaling pathway and up-regulate the expression of ZO-1 against arsenic-induced cell damage. This study provides a new perspective for understanding the heavy metal detoxification of SBSG on the intestinal and indicates that SBSG could be used as natural antioxidant resistant to heavy metal toxicity.