Berberine prevents stress-induced gut inflammation and visceral hypersensitivity and reduces intestinal motility in rats  

作　　者：Zhi-Chao Yu Yong-Xin Cen Ben-Hua Wu Cheng Wei Feng Xiong De-Feng Li Ting-Ting Liu Ming-Han Luo Li-Liangzi Guo Ying-Xue Li Li-Sheng Wang Jian-Yao Wang Jun Yao 

机构地区：[1]Department of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People’s Hospital, Shenzhen 518020, Guangdong Province, China [2]Department of Gastroenterology, Foshan Gaoming Affiliated Hospital of Guangdong Medical University, Foshan 528500, Guangdong Province, China [3]Department of General Surgery, Shenzhen Children’s Hospital, Shenzhen 518026, Guangdong Province, China

出　　处：《World Journal of Gastroenterology》2019年第29期3956-3971,共16页世界胃肠病学杂志（英文版）

基　　金：the National Natural Science Foundation of China,No.81800489;Shenzhen Health and Family Planning System Research Project,No.SZXJ2017030;Technical Research and Development Project of Shenzhen,Nos.JCYJ20170307100538697 and JCYJ20170307100911479

摘　　要：BACKGROUND Irritable bowel syndrome (IBS) is a common chronic non-organic disease of the digestive system. Berberine (BBR) has been used to treat patients with IBS, but the underlying therapeutic mechanism is little understood. We believe that BBR achieves its therapeutic effect on IBS by preventing stress intestinal inflammation and visceral hypersensitivity and reducing bowel motility. AIM To test the hypothesis that BBR achieves its therapeutic effect on IBS by preventing subclinical inflammation of the intestinal mucosa and reducing visceral hypersensitivity and intestinal motility. METHODS IBS was induced in rats via water avoidance stress (WAS). qRT-PCR and histological analyses were used to evaluate the levels of cytokines and mucosal inflammation, respectively. Modified ELISA and qRT-PCR were used to evaluate the nuclear factor kappa-B (NF-κB) signal transduction pathway. Colorectal distention test, gastrointestinal transit measurement, Western blot, and qRT-PCR were used to analyze visceral sensitivity, intestinal motility, the expression of Ckit (marker of Cajal mesenchymal cells), and the expression of brain derived neurotrophic factor (BDNF) and its receptor TrkB.RESULTS WAS led to mucosal inflammation, visceral hyperalgesia, and high intestinal motility. Oral administration of BBR inhibited the NF-κB signal transduction pathway, reduced the expression of pro-inflammatory cytokines [interleukin (IL)- 1β, IL-6, interferon-γ, and tumor necrosis factor-α], promoted the expression of anti-inflammatory cytokines (IL-10 and transforming growth factor-β), and improved the terminal ileum tissue inflammation. BBR inhibited the expression of BDNF, TrkB, and C-kit in IBS rats, leading to the reduction of intestinal motility and visceral hypersensitivity. The therapeutic effect of BBR at a high dose (100 mg/kg) was superior to than that of the low-dose (25 mg/kg) group. CONCLUSION BBR reduces intestinal mucosal inflammation by inhibiting the intestinal NF-κB signal pathway in the IBS rats. BBR reduces the BACKGROUND Irritable bowel syndrome(IBS) is a common chronic non-organic disease of the digestive system. Berberine(BBR) has been used to treat patients with IBS, but the underlying therapeutic mechanism is little understood. We believe that BBR achieves its therapeutic effect on IBS by preventing stress intestinal inflammation and visceral hypersensitivity and reducing bowel motility.AIM To test the hypothesis that BBR achieves its therapeutic effect on IBS by preventing subclinical inflammation of the intestinal mucosa and reducing visceral hypersensitivity and intestinal motility.METHODS IBS was induced in rats via water avoidance stress(WAS). qRT-PCR and histological analyses were used to evaluate the levels of cytokines and mucosal inflammation, respectively. Modified ELISA and qRT-PCR were used to evaluate the nuclear factor kappa-B(NF-κB) signal transduction pathway. Colorectal distention test, gastrointestinal transit measurement, Western blot, and qRT-PCR were used to analyze visceral sensitivity, intestinal motility, the expression of Ckit(marker of Cajal mesenchymal cells), and the expression of brain derived neurotrophic factor(BDNF) and its receptor TrkB.RESULTS WAS led to mucosal inflammation, visceral hyperalgesia, and high intestinal motility. Oral administration of BBR inhibited the NF-κB signal transduction pathway, reduced the expression of pro-inflammatory cytokines [interleukin(IL)-1β, IL-6, interferon-γ, and tumor necrosis factor-α], promoted the expression of anti-inflammatory cytokines(IL-10 and transforming growth factor-β), and improved the terminal ileum tissue inflammation. BBR inhibited the expression of BDNF, TrkB, and C-kit in IBS rats, leading to the reduction of intestinal motility and visceral hypersensitivity. The therapeutic effect of BBR at a high dose(100 mg/kg) was superior to than that of the low-dose(25 mg/kg) group.CONCLUSION BBR reduces intestinal mucosal inflammation by inhibiting the intestinal NF-κB signal pathway in the IBS rats. BBR reduces the expression of

关 键 词：IRRITABLE bowel syndrome Visceral hypersensitivity BERBERINE RIFAMPICIN Nuclear FACTOR KAPPA-B BRAIN-DERIVED neurotrophic FACTOR Cajal mesenchymal cells Ckit 

分 类 号：R[医药卫生]