Gut microbiota drives the attenuation of dextran sulphate sodium-induced colitis by Huangqin decoction
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Yang Yang1,2,3,*, Gang Chen1,2,4,*, Qian Yang1,2,6,*, Juan Ye1,2, Xueting Cai1,2, Pamo Tsering5, Xiaolan Cheng1,2, Chunping Hu1,2, Shuangquan Zhang6 and Peng Cao1,2
1Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210028, Jiangsu, China
2Laboratory of Cellular and Molecular Biology, Jiangsu Province Academy of Traditional Chinese Medicine, Nanjing 210028, Jiangsu, China
3State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210097, China
4School of Pharmacy, China Pharmaceutical University, Nanjing 210009, China
5Hainan Tibetan Autonomous Prefecture Tibetan Medical Hospital, Gonghe 813099, China
6School of Life Science, Nanjing Normal University, Nanjing 210046, China
*These authors contributed equally to this work
Peng Cao, email: firstname.lastname@example.org
Keywords: Huangqin decoction, ulcerative colitis, gut microbiota, high-throughput sequencing
Received: January 10, 2017 Accepted: March 14, 2017 Published: March 22, 2017
The gut microbiota, including probiotics and pathogenic microorganisms, is involved in ulcerative colitis (UC) by regulating pathogenic microorganisms and the production of intestinal mucosal antibodies. Huangqin decoction (HQD), a traditional Chinese formula chronicled in the Shanghan lun, has been recognized as an effective drug for UC, owing to its anti-inflammatory and anti-oxidative properties. In the present study, we investigated whether HQD ameliorates dextran sulphate sodium (DSS)-induced colitis through alteration of the gut microbiota. We found that HQD significantly inhibited colitis, alleviating the loss of body weight, disease activity index, colon shortening, tissue injury, and inflammatory cytokine changes induced by DSS treatment. Principal component analysis and principal co-ordinate analysis showed an obvious difference among the groups, with increased diversity in the DSS and DSS+HQD groups. Linear discriminant analysis effect size was used to determine differences between the groups. The relative abundance of Lactococcus was higher in the DSS+HQD group than in the DSS group, whereas Desulfovibrio and Helicobacter were decreased. Furthermore, the protective effect of HQD was attenuated only in antibiotic-treated mice. In conclusion, our results suggest that HQD could ameliorate DSS-induced inflammation through alteration of the gut microbiota.
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