Cheng Jing, Lü Shangbin, Zhang Yi, H U Shuangyuan, Wei Pengfei, Zhou Wenhua, Shi Junfeng
{"title":"Efficacy of Qifu Lizhong enema prescription on intestinal mucosal tight junction function modulation of ulcerative colitis rat model.","authors":"Cheng Jing, Lü Shangbin, Zhang Yi, H U Shuangyuan, Wei Pengfei, Zhou Wenhua, Shi Junfeng","doi":"10.19852/j.cnki.jtcm.20220922.002","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To investigate the efficacy and mechanism of Qifu Lizhong enema prescription(, QFLZ) on intervening ulcerative colitis (UC) rat model with TCM spleen and kidney insufficiency syndrome.</p><p><strong>Methods: </strong>Seventy-two male Sprague-Dawley rats were randomly assigned to six groups: normal model, mesalazine, and QFLZ high, medium, and low dose groups, each with 12 rats. After 3 d of adaptation feeding, all groups except the normal group were induced using rhubarb decoction in combination with trinitrobenzene sulfonic acid (TNBS)/55 % ethanol to establish a UC rat model. Following successful modeling, the normal and model groups received daily saline enema, while the Chinese medicine and Western medicine groups received daily QFLZ and Mesalazine enema for 2 weeks respectively. The disease activity index score, hematoxylin and eosin staining, immunohistochemistry, and Western blotting were used to determine the expression of claudin 1, claudin 2, zonula occludens-1 protein (ZO-1), and F-actin proteins in each rat colon tissue following treatment.</p><p><strong>Results: </strong>QFLZ significantly alleviated the structural disorganization in the form of epithelial glands in the intestinal mucosa of rats with UC and retarded the progression of the disease. The intestinal mucosal epithelial cells of UC rats showed decreased expression of claudin 1, ZO-1, F-actin ( 0.05), claudin 2 appeared elevated ( 0.05), which resulted in impaired TJ. Treatment with QFLZ resulted in elevated expression of claudin 1 ( 0.05), ZO-1 ( 0.05) and F-actin ( 0.05) and decreased expression of claudin 2 ( 0.05), which allowed for repair of the intestinal mucosal TJ, which in turn served as a treatment for UC.</p><p><strong>Conclusions: </strong>The mechanism of repairing TJ function and repairing the intestinal mucosal barrier by QFLZ may be associated with up-regulation of claudin 1, ZO-1, and F-actin levels, and down-regulation of claudin 2 expression level.</p>","PeriodicalId":17450,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10012196/pdf/JTCM-43-2-303.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.19852/j.cnki.jtcm.20220922.002","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: To investigate the efficacy and mechanism of Qifu Lizhong enema prescription(, QFLZ) on intervening ulcerative colitis (UC) rat model with TCM spleen and kidney insufficiency syndrome.
Methods: Seventy-two male Sprague-Dawley rats were randomly assigned to six groups: normal model, mesalazine, and QFLZ high, medium, and low dose groups, each with 12 rats. After 3 d of adaptation feeding, all groups except the normal group were induced using rhubarb decoction in combination with trinitrobenzene sulfonic acid (TNBS)/55 % ethanol to establish a UC rat model. Following successful modeling, the normal and model groups received daily saline enema, while the Chinese medicine and Western medicine groups received daily QFLZ and Mesalazine enema for 2 weeks respectively. The disease activity index score, hematoxylin and eosin staining, immunohistochemistry, and Western blotting were used to determine the expression of claudin 1, claudin 2, zonula occludens-1 protein (ZO-1), and F-actin proteins in each rat colon tissue following treatment.
Results: QFLZ significantly alleviated the structural disorganization in the form of epithelial glands in the intestinal mucosa of rats with UC and retarded the progression of the disease. The intestinal mucosal epithelial cells of UC rats showed decreased expression of claudin 1, ZO-1, F-actin ( 0.05), claudin 2 appeared elevated ( 0.05), which resulted in impaired TJ. Treatment with QFLZ resulted in elevated expression of claudin 1 ( 0.05), ZO-1 ( 0.05) and F-actin ( 0.05) and decreased expression of claudin 2 ( 0.05), which allowed for repair of the intestinal mucosal TJ, which in turn served as a treatment for UC.
Conclusions: The mechanism of repairing TJ function and repairing the intestinal mucosal barrier by QFLZ may be associated with up-regulation of claudin 1, ZO-1, and F-actin levels, and down-regulation of claudin 2 expression level.
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