Scope: The over-activation of the nucleotide-binding domain like receptor protein 3 (NLRP3) inflammasome plays an important role in the pathogenesis of ulcerative colitis (UC). Chlorogenic acid (CGA) exposure is identified as an effective strategy for repressing inflammatory responses. Methods and results: In this study, the NLRP3 inflammasome model with LPS/ATP-induced RAW264.7 cells in vitro and dextran-sulfate-sodium (DSS)-induced colitis in mice are used to evaluate the effect of CGA on NLRP3 inflammasome-related signaling. The results suggest that CGA suppressed the expression of NLRP3 inflammasome-related genes (apoptosis-associated speck-like protein containing CARD (ASC), cysteine-requiring aspartate protease (Caspase)-1 p45, Caspase-1 p20, pro-/cleaved-interleukin (IL)-1 , pro-/cleaved-IL-18), p-nuclear factor kappa B (NF-B) protein, and miR-155 in mice with colitis. Gain-and loss-of-function studies of miR-155 are performed to elucidate its role in inflammation. Moreover, activation of the NF-B/NLRP3 inflammasome pathway and miR-155 expression is investigated. CGA exposure in lipopolysaccharide (LPS)/adenosine triphosphate (ATP)-stimulated RAW264.7 cells leads to a decrease in p-NK-B and NLRP3 inflammasome-related proteins, which is dependent on the downregulation of miR-155 expression. Conclusions: These findings indicate that CGA prevented colitis by downregulating miR-155 expression and inactivating the NF-B/NLRP3 inflammasome pathway in macrophages. The current study has promising therapeutic implications in the treatment of UC.

Nonalcoholic fatty liver disease (NAFLD) has received worldwide scientific attention because of its rapidly increasing prevalence, and it has emerged as a serious public health problem in end-stage liver disease. Many factors are involved in the multifactorial development and progression of liver disease by influencing multiple signaling and metabolic pathways. Currently, many studies have demonstrated the critical role of microRNA-21 (miR-21) in NAFLD pathogenesis. In addition, many studies have found that miR-21 is highly expressed in inflammatory bowel disease, which is associated with intestinal barrier dysfunction and altered gut microbiota. In this paper, we focus on the regulatory role of miR-21 in the progression of NAFLD and its effect on the gut microbiota, summarize the involvement of miR-21 through a variety of signaling pathways and metabolic pathways, as well as discuss some predicted miR-21 target genes and miR-21 pathways for future experimental identification.