[rCsHscB derived from Clonorchis sinensis has therapeutic effect on dextran sodium sulfate-induced chronic ulcerative colitis in mice].

OBJECTIVE: To investigate the therapeutic effect of rCsHscB derived from Clonorchis sinensis on dextran sodium sulfate (DSS)-induced chronic ulcerative colitis in mice. OBJECTIVE: C57BL/6 mice were randomized into negative control (NC) group (n= 10), rCsHscB group (n=10), DSS group (n=15), and DSS+rCsHscB group (n=15), and in the latter two groups, chronic ulcerative colitis was induced in the mice using 2% DSS. In rCsHscB and DSS+ rCsHscB groups, the mice received intraperitoneal injections of 125 μg/mL rCsHscB on the 4th and 7th day following DSS administration, and PBS was injected in the other two groups. The mice were euthanized on the 84th day, and pathological changes of the colon were evaluated by HE and Masson staining. The levels of CD4(+) and CD8(+) T cells in the peripheral blood and lamina propria gastric lymphocytes (LPL) were analyzed by flow cytometer; the levels of IL-6, MCP-1 and IL-10 in colon homogenate were determined using ELISA, and the phosphorylation of ERK1/2, JNK and P38 was detected with Western blotting. OBJECTIVE: Compared with those in NC group, the mice in rCsHscB group exhibited no adverse responses to the treatment. The mice in DSS group had severe pathologies in the colon with significantly increased ratios of CD4(+) and CD4(+)/CD8(+) T cells in peripheral blood and LPL, increased levels of IL-6 and MCP-1 but no obvious changes in IL-10 in colon homogenate, and significantly augmented phosphorylation levels of ERK1/2, JNK and P38. Compared with those in DSS group, the mice in DSS+ rCsHscB group showed ameliorated colon pathologies with decreased CD4(+)T/CD8(+)T cell ratio in the peripheral blood and LPL, significantly decreased IL-6 and MCP-1 levels and increased IL-10 in colon homogenate, and lowered phosphorylation levels of ERK1/2, JNK and P38. OBJECTIVE: rCsHscB can produce therapeutic effect on DSS-induced chronic ulcerative colitis in mice possibly by inhibiting the production of pro-inflammatory factors and regulating the balance of CD4(+)/CD8(+)T cells through the MAPK pathway.