Qi Lian Jie Ning Ameliorates DSS-Induced Colitis in Rats by Inhibition of JAK2/STAT3 and TLR4/NF-kB Pathways.

Ulcerative colitis (UC) is a clinically common idiopathic inflammatory bowel disease. The DSS-induced colitis model was induced via 5% DSS for 7 days. Rats were gavaged with QLJCN solution in different concentrations. This study measured body weight, colon length, and DAI of rats in each group. The hematoxylin-eosin staining assessed the histopathology and histological score. Western blot analysis examined the expressions of TFF3, MUC-2, JAK2/STAT3 pathway-, and TLR4/NF-κB pathway-related markers. Moreover, the contents of IL-6, TNF-α, and LPS in the colons/serum were determined by ELISA. TLR4 activator (RS09) or JAK2/STAT3 activator (colivelin) were employed for the rescue experiments. QLJCN repressed weight loss and the increase of DAI score in DSS rats. QLJCN also increased the colon length and alleviated colonic damage, and effectively repressed the levels of IL-6 and TNF-α but elevated the levels of TFF3 and MUC-2 in the colons/serum of DSS rats. Moreover, QLJCN weakened the activation of JAK2/STAT3 and TLR4/NF-κB pathways, and alleviated the intestinal inflammation. Furthermore, these ameliorative effects of QLJCN were reversed by TLR4 activator (RS09) or JAK2/STAT3 activator (colivelin). QLJCN has protective effects on DSS-induced colitis rats by restraining JAK2/STAT3 and TLR4/NF-κB pathways. This study provides new therapeutic strategies for UC.