Abstract
Inflammatory bowel disease (IBD) is one of the predominant intestinal diseases associated with chronic inflammation and ulceration of the colon. This study explored the ameliorative effect of Aloe vera extract (Aloe) and/or heat-killed Lactobacillus plantarum L.137 (HK L.137) on dextran sodium sulfate (DSS)-induced colitis in mice. Aloe and/or HK L.137 were supplied for 9 days and the mice were challenged with DSS for 7 days. The DSS group demonstrated bloody diarrhea, colitis of high histologic grade, increased nuclear factor-kappa B (NF-κB) p65, inducible nitric oxide synthase (iNOS), myeloperoxidase (MPO), interleukin (IL)-6, and tumor necrosis factor (TNF)-α, and decreased IL-10 expression. These alterations were dwindled in DSS-induced mice treated with Aloe and HK L.137 separately. Aloe and HK L.137 together have augmented the therapeutic effect of each other. In conclusion, our findings demonstrated that Aloe and/or HK L.137 ameliorated DSS-induced colitis by promoting the secretion of anti-inflammatory cytokines and suppressing pro-inflammatory mediators. This study indicated that A. vera may function synergistically with HK L.137 to confer an effective strategy to prevent colitis.
Highlights
Inflammatory bowel disease (IBD) is a chronic immune-mediated disease characterized by inflammation and ulceration of mucosal and submucosal layers of the colon
Mice received dextran sodium sulfate (DSS) showed an increase in Disease Activity Index (DAI) when compared with the control group (p < 0.001)
DSS is frequently used in the induction of IBD and investigation of different treatment trials [23,28]
Summary
Inflammatory bowel disease (IBD) is a chronic immune-mediated disease characterized by inflammation and ulceration of mucosal and submucosal layers of the colon. The etiology of the disease is not precisely known; several different genetic and environmental factors might be involved [1]. IBDs include two basic types, namely Crohn’s disease (CD) and ulcerative colitis (UC). The disease is manifested by chronic diarrhea, rectal bleeding, and abdominal cramps [2]. A vast number of inflammatory mediators were implicated in the pathogenesis of the disease.
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