Abstract
Andrographolide is a traditional herb medicine, widely used in Asia for conditions involving inflammation. The andrographlide-lipoic acid conjugate, AL-1, has been found being able to alleviate inflammation in our previous reports. Although the anti-inflammatory activity of AL-1 contributes to its cytoprotective effects, whether AL-1 can improve inflammatory bowel disease (IBD) and the underlying mechanisms of its action remain largely unknown. In this study, we investigated the anti-inflammatory effects of AL-1 in C57BL/6 mice with trinitrobenzenesulfonic acid (TNBS)-induced colitis. The body weight loss and length change of colon after TNBS instillation were more severe than those in normal mice. AL-1 treatment led to significant reductions in disease activity index (DAI), macroscopic score and colon mucosa damage index (CMDI) associated with TNBS administration. AL-1 inhibited the inflammatory response via lowering the level of inflammatory cytokines and myeloperoxidase (MPO) activity. AL-1 attenuated the expression of p-p65, p-IκBα and COX-2 in the colitis mice. The alleviation of colon injury by AL-1 treatment was also evidenced by the increased expression of PPAR-γ. These results indicated that AL-1 could protect intestinal tract from the injury induced by TNBS in mice, suggesting that AL-1 may have potential in treatment for IBD.
Highlights
Andrographolide is a traditional herb medicine, widely used in Asia for conditions involving inflammation
In order to examine whether AL-1 could improve the clinical symptoms of trinitrobenzenesulfonic acid (TNBS)-induced colitis in mice, the clinical signs including weight changes, colon length, disease activity index (DAI) score and macroscopic score were assessed
The significant weight loss, DAI score and macroscopic score and shortening colon length in model group manifested that colon instillation of TNBS resulted in a reproducible colitis in mice (Fig. 2A–F)
Summary
Andrographolide is a traditional herb medicine, widely used in Asia for conditions involving inflammation. We investigated the anti-inflammatory effects of AL-1 in C57BL/6 mice with trinitrobenzenesulfonic acid (TNBS)-induced colitis. The alleviation of colon injury by AL-1 treatment was evidenced by the increased expression of PPAR-γ These results indicated that AL-1 could protect intestinal tract from the injury induced by TNBS in mice, suggesting that AL-1 may have potential in treatment for IBD. Once the homeostasis breaks down and shifts to the pro-inflammatory side, hyperactive immune cells secrete the pro-inflammatory cytokines including TNF-α, IL-1βand IL-6 through the activation of regulatory mechanisms such as the NF-κB and PPAR-γpathways[5,6,7] These signaling cascades would increase people’s susceptibility to IBD and eventually precipitate the chronic inflammatory pathology found in the disease. We investigated the therapeutic effects and mechanisms of AL-1 in TNBS-induced colitis in mice
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