Sinapic Acid(SA) attnuated the DSS-induced inestinal fibrosis in C57/6BL mice by modulated the NLRP3 inflammasome activation and autophagy pathway

다국어 초록 (Multilingual Abstract)

To observe the effect of SA on DSS-induced intestinal fibrosis in mice. The mice were randomly divided into normal, DSS and SA treated DSS mice group. Changes in body weight(BW), blood stool and diarrhea were observed. The serum levels of IL-1β, IL-6, IL-17A, IL-18 and TNF-α were determined by ELISA kits. The protein levels of NLRP3, caspase-1, ASC, IL-1 β, α-SMA, CollagenI, Beclin1, LC3II/I and p62 were detected by Western Blotting assay. Compared with the normal group, SA significantly inhibited the loss of BW and DAI score in colitis mice (P<0.05). H&E and Masson staining assay suggested the SA reduced epithelial cell damage, crypt structure loss, inflammatory cell infiltration, and the fibrogenesis in colon of colitis mice. The serum levels of IL-1β, IL-6, IL-17A, IL-18 and TNF-α were decreased by SA(P<0.05). SA was able to reduce the protein levels of NLRP3, Caspase-1, ASC, IL-1β, α-SMA, Collagen-I, p62, and increased the expressions of Beclin1 and LC3II/I in colitis mice. The study demonstrated that SA can modulate the activity of NLRP3 inflammasome and autophagy pathway to improve DSS induced intaestinal fibrosis in mice.