Curcumin ameliorates dextran sulfate sodium-induced colitis in mice via regulation of autophagy and intestinal immunity

Abstract

Background/Aims: Inflammatory bowel disease (IBD) is regarded as a kind of chronic and unspecific intestinal inflammatory disorder. Its exact pathogenesis has not been elucidated. Curcumin, as an herbal drug, has been used in the treatment of IBD due to its immu-noregulation. Autophagy has been reported to play an important role in the mechanism of IBD. In the present study, we focused on the autophagic regulation role of curcumin in the murine model of dextran sulfate sodium (DSS)-induced colitis. Materials and Methods: We investigated the effects of curcumin on the progress of DSS-induced acute colitis in mice by evaluating the disease activity index (DAI) and histopathological score. Meanwhile, the mRNA and protein expression of autophagy-related key genes from colon tissues comprising autophagy-related 5 (ATG5), LC3-phosphatidylethanolamine conjugate (LC-3II), beclin-1, and B cell lymphoma 2 (bcl-2) was examined by quantitative reverse transcription polymerase chain reaction and Western blot. Furthermore, the mRNA and protein expression of cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL) 6, IL-10, and IL-17A, was examined. Autophagosome was also examined under transmission electron microscopy. Results: Both DAI and histopathological score increased in mice with DSS-induced colitis and obviously decreased after curcumin intervention. The expression levels of TNF-α, IL-6, IL-17, ATG5, LC-3II, and beclin-1 were significantly higher in mice with colitis than in normal ones, whereas those of IL-10 and bcl-2 decreased accordingly. However, curcumin intervention adjusted the expression level of those factors toward normal level. The number of autophagosome in the colon epithelia increased after DSS stimulation and decreased after curcumin administration. Conclusion: Curcumin could prevent the development of DSS-induced colitis through the inhibition of excessive autophagy and regulation of following cytokine networks.