Renshen (Radix Ginseng) polysaccharide promotes repair of the mice intestinal mucosa through regulatory mechanisms based on polyamine and human antigen R.

Wang Guanyu, Dai Xingzhen, Liu Yiting, Zhu Zeming, H U Ling, L I Ruliu
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Abstract

Objective: To investigate the mechanism and effect of Renshen (Radix Ginseng) polysaccharide on the migration of intestinal epithelial cell line 6 (IEC-6), as well as the repair mechanism of Renshen (Radix Ginseng) polysaccharide on colonic injury induced by dextran sulfate sodium (DSS) in mice.

Methods: Mice were fed 3% (w/v) DSS for 6 d to create colonic lesions. A cell-migration model was created using cell scratching. mRNA expression, protein expression, translation efficiency of mRNA, and nucleoplasmic distribution of human antigen R (HuR) were determined by real-time reverse transcription-quantitative polymerase chain reaction, western blotting, a dual luciferase reporter system, and immunofluorescence staining, respectively.

Results: Renshen (Radix Ginseng) polysaccharide promoted the migration of IEC-6 cells and affected expression of stromal interaction molecule 1 (STIM1) and cell division cycle 42 (Cdc42) at transcriptional and post-transcriptional levels.

Conclusions: Renshen (Radix Ginseng) polysaccharide-induced repair of intestinal mucosal injury may be mediated by increased cell migration via polyamine-based regulatory mechanisms. In vitro and in vivo experiments suggest that Renshen (Radix Ginseng) polysaccharide-induced post-transcriptional regulation of STIM1 and Cdc42 may be related to differences in the regulation of different target genes by HuR. Taken together, these data provide a reference for further exploration of the protective effect of Renshen (Radix Ginseng) on the intestinal mucosa.

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人参多糖通过基于多胺和人抗原R的调控机制促进小鼠肠黏膜修复。
目的:探讨人参多糖对小肠上皮细胞系6 (IEC-6)迁移的影响机制及人参多糖对硫酸葡聚糖钠(DSS)所致小鼠结肠损伤的修复作用机制。方法:小鼠灌胃3% (w/v) DSS 6 d,形成结肠病变。利用细胞抓痕法建立了细胞迁移模型。分别采用实时逆转录-定量聚合酶链反应、western blotting、双荧光素酶报告系统和免疫荧光染色检测mRNA表达、蛋白表达、mRNA翻译效率和人抗原R (HuR)的核质分布。结果:人参多糖在转录和转录后水平上促进IEC-6细胞的迁移,影响基质相互作用分子1 (STIM1)和细胞分裂周期42 (Cdc42)的表达。结论:人参多糖对肠黏膜损伤的修复作用可能通过多胺调节机制介导细胞迁移的增加。体外和体内实验表明,人参多糖诱导的STIM1和Cdc42转录后调控可能与HuR对不同靶基因调控的差异有关。综上所述,这些数据为进一步探索人参对肠黏膜的保护作用提供了参考。
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