Anti-inflammation of Erianin in dextran sulphate sodium-induced ulcerative colitis mice model via collaborative regulation of TLR4 and STAT3.

Ulcerative colitis (UC) is a chronic, idiopathic and inflammatory disease of the rectal and colonic mucosa. Studies have shown that Toll-like receptors (TLR) 4 and Signal Transducer and Activator of Transcription 3 (STAT3)-mediated the decline in immune function and inflammatory infiltration are potential pathomechanism of UC occurrence and development. In this study, the anti-inflammation of Erianin, a natural bibenzyl compound with the antioxidant, antitumor, and anti-inflammatory activities, was investigated in a dextran sodium sulphate-induced UC mouse model. Three-week Erianin administration resulted in the increment on the body weight and colon length, and the reduction on the activity index score of UC mice. Liver, spleen, and renal organ indexes and pathological observations confirmed that Erianin was not cytotoxic and had an effect of improving immune organ function. The haematoxylin and eosin staining sections of colon tissue show Erianin's effect of reversing inflammation in the mucosal laye. Proteomic analysis and enzyme-linked immunosorbent assay indicated that Erianin regulated the levels of inflammatory and oxidative stress-related factors and immunochemokines in serum and colon tissues thereby reducing cell peroxidative damage and reducing immune inflammatory responses. Further data obtained by Western Blotting confirmed that Erianin's anti-UC activity was mediated by inhibiting the TLR4 and STAT3 signaling.