Bu-Gao Zhou1, Fu-Chun Liu2, Hai-Mei Zhao3, Xiao-Yun Zhang4, Hai-Yan Wang5, Duan-Yong Liu6. 1. Office of Academic Research, Jiangxi University of Traditional Chinese Medicine, Nanchang, 330004, Jiangxi Province, China. Electronic address: 924043571@qq.com. 2. Department of Postgraduate, Jiangxi University of Traditional Chinese Medicine, Nanchang, 330004, Jiangxi Province, China. Electronic address: 1912318114@qq.com. 3. College of Traditional Chinese Medicine, Jiangxi University of Traditional Chinese Medicine, Nanchang, 330004, Jiangxi Province, China. Electronic address: 20050852@jxutcm.edu.cn. 4. Department of Postgraduate, Jiangxi University of Traditional Chinese Medicine, Nanchang, 330004, Jiangxi Province, China. Electronic address: 1647310731@qq.com. 5. Doctoral Candidate of 2017, Jiangxi University of Traditional Chinese Medicine, Nanchang, 330004, Jiangxi Province, China. Electronic address: 378278287@qq.com. 6. Science and Technology College, Jiangxi University of Traditional Chinese Medicine, Nanchang, 330004, Jiangxi Province, China; Formula-Pattern Research Center of Jiangxi, Nanchang, 330004, Jiangxi Province, China. Electronic address: 20050850@jxutcm.edu.cn.
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: As a classic prescription and commercial Chinese patent medicine, Zuojin Pill (ZJP) has been used to treat ulcerative colitis (UC) effectively for many years. However, its mechanism of action remains unclear. AIM OF THE STUDY: METHODS: Mice with dextran-sulfate-sodium-induced colitis were treated with ZJP for 7 d. In the present study, the therapeutic effect of ZJP was evaluated by macroscopic and microscopic observation; regulatory T (Treg) cells and their subsets were analyzed by flow cytometry; and the composition of gut microbiota was tested by 16S rRNA analysis. Activation of the phosphoinostide 3-kinase (PI3K)/Akt signaling pathway was observed by western blotting. RESULTS: The pathological damage was attenuated and expression of proinflammatory cytokines was decreased. While the diversity of intestinal microflora was regulated, the relative abundance of Actinobacteria, and Sphingobacteriia was modified. Meanwhile, the level of CD4+CD25+Foxp3+ and PD-L1+ Treg cells improved. These changes maintained a positive correlation which was analyzed statistically. Our results also showed that ZJP inhibited activation of the PI3K/Akt signaling pathway. CONCLUSIONS: ZJP regulates crosstalk between intestinal microflora and Treg cells to attenuate experimental colitis via the PI3K/Akt signaling pathway.
ETHNOPHARMACOLOGICAL RELEVANCE: As a classic prescription and commercial Chinese patent medicine, Zuojin Pill (ZJP) has been used to treat ulcerative colitis (UC) effectively for many years. However, its mechanism of action remains unclear. AIM OF THE STUDY: METHODS:Mice with dextran-sulfate-sodium-induced colitis were treated with ZJP for 7 d. In the present study, the therapeutic effect of ZJP was evaluated by macroscopic and microscopic observation; regulatory T (Treg) cells and their subsets were analyzed by flow cytometry; and the composition of gut microbiota was tested by 16S rRNA analysis. Activation of the phosphoinostide 3-kinase (PI3K)/Akt signaling pathway was observed by western blotting. RESULTS: The pathological damage was attenuated and expression of proinflammatory cytokines was decreased. While the diversity of intestinal microflora was regulated, the relative abundance of Actinobacteria, and Sphingobacteriia was modified. Meanwhile, the level of CD4+CD25+Foxp3+ and PD-L1+ Treg cells improved. These changes maintained a positive correlation which was analyzed statistically. Our results also showed that ZJP inhibited activation of the PI3K/Akt signaling pathway. CONCLUSIONS:ZJP regulates crosstalk between intestinal microflora and Treg cells to attenuate experimental colitis via the PI3K/Akt signaling pathway.