Abstract
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.
Highlights
Inflammatory bowel disease (IBD) is a group of inflammatory conditions of the colon and small intestine that includes ulcerative colitis (UC) and Crohn’s disease (CD) [1]
The administration of Huangqin decoction (HQD), significantly suppressed the accumulation of Tumour necrosis factor alpha (TNF-α), Interleukin 6 (IL-6), Interleukin 1 beta (IL-1β), and COX-2 in the colon tissues of mice with dextran sulphate sodium (DSS)-induced colitis. These results suggest that HQD is capable of preventing DSSinduced colitis (Figure 1F)
Many studies have shown that UC is associated with genetic and environment factors that lead to impairment of the intestinal mucosal barrier
Summary
Inflammatory bowel disease (IBD) is a group of inflammatory conditions of the colon and small intestine that includes ulcerative colitis (UC) and Crohn’s disease (CD) [1]. UC mainly begins in the rectum, spreads proximally in a continuous fashion, and frequently involves the periappendiceal region. It is characterized by acute pain, vomiting, weight loss, diffuse mucosal inflammation, diarrhoea, and bloody stools [2, 3]. Coexistence between the host and the gut microbiota helps to shape the mucosal and www.impactjournals.com/oncotarget systemic immune systems. When the gut microbiota invades intestinal tissue and induces local or systemic inflammation, the mucosal immune system has a number of protective mechanisms that allow the host to mount an appropriate immune response to invading bacteria [6]. The intestinal microbiota is considered to be a significant factor in the aetiology of IBD [7]
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