Su Hang, Tan Yujing, Zhou Zhijiang, Wang Chunjuan, Chen Wei, Wang Jinlong, Sun Haiming
College of Science, Traditional Chinese Medicine Biotechnology Innovation Center in Jilin Province, Beihua University, Jilin 132013, P.R. China.
School of Pharmacy, Beihua University, Jilin 132000, P.R. China.
Exp Ther Med. 2023 Jun 16;26(2):369. doi: 10.3892/etm.2023.12068. eCollection 2023 Aug.
Inflammatory bowel disease (IBD) is a chronic recurrent gastrointestinal disease that seriously endangers human and animal health. Although the etiology of IBD is complex and the pathogenesis is not well understood, studies have found that genetic predisposition, diet and intestinal flora disorders are the main risk factors for IBD. The potential biological mechanism of total ginsenosides (TGGR) in the treatment of IBD remains to be elucidated. Surgery is still the main strategy for the treatment of IBD, due to the relatively high side effects of related drugs and the easy development of drug resistance. The purpose of the present study was to evaluate the efficacy of TGGR and explore the effect of TGGR on the intestinal inflammation induced by sodium dodecyl sulfate (SDS) in and to initially explain the improvement effect and mechanism of TGGR on enteritis by analyzing the levels of -related proteins. During the experiment, the survival rate, climb index and abdominal characteristics of the was recorded. Intestinal samples of were collected for analysis of intestinal melanoma. The oxidative stress related indexes of catalase, superoxide dismutase and malondialdehyde were determined by spectrophotometry. Western blotting detected the expression of signal pathway-related factors. The effects of TGGR on growth indices, tissue indices, biochemical indices, signal pathway transduction and related mechanisms of SDS-induced enteritis model were studied. The results showed that TGGR could repair SDS-induced enteritis of through MAPK signaling pathway, improve survival rate and climbing ability and repair intestinal damage and oxidative stress damage. The results suggested that TGGR has potential application value in the treatment of IBD and its mechanism is related to the downregulation of phosphorylated (p)-JNK/p-ERK levels, which provides a basis for drug research in the treatment of IBD.
炎症性肠病（IBD）是一种严重危害人类和动物健康的慢性复发性胃肠道疾病。尽管IBD的病因复杂且发病机制尚不完全清楚，但研究发现遗传易感性、饮食和肠道菌群紊乱是IBD的主要危险因素。人参总皂苷（TGGR）治疗IBD的潜在生物学机制仍有待阐明。由于相关药物副作用相对较高且易产生耐药性，手术仍是IBD的主要治疗策略。本研究旨在评估TGGR的疗效，探讨TGGR对十二烷基硫酸钠（SDS）诱导的肠炎的影响，并通过分析相关蛋白水平初步解释TGGR对肠炎的改善作用及机制。实验过程中，记录小鼠的存活率、攀爬指数和腹部特征。采集小鼠肠道样本用于肠道黑色素瘤分析。采用分光光度法测定过氧化氢酶、超氧化物歧化酶和丙二醛等氧化应激相关指标。蛋白质免疫印迹法检测信号通路相关因子的表达。研究TGGR对SDS诱导的小鼠肠炎模型的生长指标、组织指标、生化指标、信号通路转导及相关机制的影响。结果表明，TGGR可通过丝裂原活化蛋白激酶（MAPK）信号通路修复SDS诱导的小鼠肠炎，提高存活率和攀爬能力，修复肠道损伤和氧化应激损伤。结果提示，TGGR在IBD治疗中具有潜在应用价值，其机制与磷酸化（p）-JNK/p-ERK水平下调有关，为IBD治疗药物研究提供了依据。
