Jin-Fen Chen1, Dan-Dan Luo2, Yin-Si Lin3, Yu-Hong Liu4, Jia-Zhen Wu5, Xiao-Qing Yi6, Yan Wu7, Qian Zhang8, Chang-Jun Gao9, Jian Cai10, Zi-Ren Su11. 1. Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, People's Republic of China. Electronic address: chenjf36@126.com. 2. Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, People's Republic of China. Electronic address: luodandan1123@163.com. 3. Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, People's Republic of China. Electronic address: lys2432519239@163.com. 4. Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, People's Republic of China. Electronic address: liuyuhong@gzucm.edu.cn. 5. Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, People's Republic of China. Electronic address: zhen3305@126.com. 6. Guangdong Academy of Forestry, Guangzhou, 510520, People's Republic of China. Electronic address: 465980167@qq.com. 7. Guangdong Academy of Forestry, Guangzhou, 510520, People's Republic of China. Electronic address: iy860814@sina.com. 8. Guangdong Academy of Forestry, Guangzhou, 510520, People's Republic of China; Guangdong Provincial Key Laboratory of Silviculture, Protection and Utilization, Guangzhou, 510520, People's Republic of China. Electronic address: zhang7610@163.com. 9. Guangdong Academy of Forestry, Guangzhou, 510520, People's Republic of China; Guangdong Provincial Key Laboratory of Silviculture, Protection and Utilization, Guangzhou, 510520, People's Republic of China. Electronic address: gaochangjun015@163.com. 10. Guangdong Academy of Forestry, Guangzhou, 510520, People's Republic of China; Guangdong Provincial Key Laboratory of Silviculture, Protection and Utilization, Guangzhou, 510520, People's Republic of China. Electronic address: caijian@sinogaf.cn. 11. Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, People's Republic of China; Dongguan Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Medicine, Dongguan, 523808, People's Republic of China. Electronic address: suziren@gzucm.edu.cn.
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: Ulcerative colitis (UC) is tightly associated with inflammation response and oxidative stress. As a folk medicine applied in treatment of diarrhea, Bruguiera gymnorrhiza also possesses anti-inflammatory and anti-oxidative activities, which indicated that B. gymnorrhiza may exert anti-colitis effect. AIM OF THE STUDY: To investigate effect and mechanism of B. gymnorrhiza on experimental UC. MATERIALS AND METHODS: Aqueous extract of B. gymnorrhiza leaves (ABL) was used for investigation in the present study. Murine UC was established through access to 3% dextran sulfate sodium (DSS) for 7 days. Meanwhile, mice accepted treatment with ABL (25, 50, 100 mg/kg) or sulfasalazine (200 mg/kg) once daily. On the last day, disease activity index (DAI) including body weight loss, fecal character and degree of bloody diarrhea was evaluated, colon segments were obtained for length measurement and further analysis and feces were collected for intestinal microbiota analysis. RESULTS: ABL ameliorated DAI scores, colon length shortening and histopathological damage in DSS-induced colitis mice obviously. SOD activity, levels of MDA and GSH altered by colitis were restored remarkably after ABL treatment. ABL inhibited increases in levels of colonic COX-2, iNOS, TNF-α, IL-6, IL-1β, IL-4, IL-10 and IL-11 in colitis mice. Moreover, ABL prominently suppressed NF-κB p65 and IκB phosphorylation and down-regulated mRNA levels of COX-2, iNOS, TNF-α, IL-6 and IL-1β elevated by colitis. As shown in microbiota analysis, ABL modulated composition of intestinal microbiota of colitis mice. CONCLUSION: ABL exhibited protective effect against DSS-induced ulcerative colitis through suppressing NF-κB activation and modulating intestinal microbiota.
ETHNOPHARMACOLOGICAL RELEVANCE: Ulcerative colitis (UC) is tightly associated with inflammation response and oxidative stress. As a folk medicine applied in treatment of diarrhea, Bruguiera gymnorrhiza also possesses anti-inflammatory and anti-oxidative activities, which indicated that B. gymnorrhiza may exert anti-colitis effect. AIM OF THE STUDY: To investigate effect and mechanism of B. gymnorrhiza on experimental UC. MATERIALS AND METHODS: Aqueous extract of B. gymnorrhiza leaves (ABL) was used for investigation in the present study. MurineUC was established through access to 3% dextran sulfate sodium (DSS) for 7 days. Meanwhile, mice accepted treatment with ABL (25, 50, 100 mg/kg) or sulfasalazine (200 mg/kg) once daily. On the last day, disease activity index (DAI) including body weight loss, fecal character and degree of bloody diarrhea was evaluated, colon segments were obtained for length measurement and further analysis and feces were collected for intestinal microbiota analysis. RESULTS:ABL ameliorated DAI scores, colon length shortening and histopathological damage in DSS-induced colitismice obviously. SOD activity, levels of MDA and GSH altered by colitis were restored remarkably after ABL treatment. ABL inhibited increases in levels of colonic COX-2, iNOS, TNF-α, IL-6, IL-1β, IL-4, IL-10 and IL-11 in colitismice. Moreover, ABL prominently suppressed NF-κB p65 and IκB phosphorylation and down-regulated mRNA levels of COX-2, iNOS, TNF-α, IL-6 and IL-1β elevated by colitis. As shown in microbiota analysis, ABL modulated composition of intestinal microbiota of colitismice. CONCLUSION:ABL exhibited protective effect against DSS-induced ulcerative colitis through suppressing NF-κB activation and modulating intestinal microbiota.