动物造模,腹泻型肠易激综合征 z-bio 2022-01-11 712

　　Objective: To investigate the immunoregulatory effect of p38MAPK signaling in diarrhea-predominant irritable bowel syndrome rats.

　　Methods: Forty SPF Wistar rats (half male and half male) were randomly divided into D-IBS model I (modeling 7d) group, II (modeling 14d), III (modeling 21d) group and blank control group. 10 per group. The model group was modeled by chronic restraint combined with senna gavage, and the blank control group was given the same volume of purified water. D-IBS rats were slaughtered on the 7th, 14th and 21st days of modeling, and the blank control group was slaughtered on the 21st day. Blood was collected from the heart, and the serum levels of IL-1β, IL-6 and TNF-α were detected by enzyme-linked immunosorbent assay (ELISA); The protein expression of p38MAPK in rat colon tissue was measured by method.

　　Results: Compared with the blank control group, the serum levels of IL-1β, IL-6 and TNF-α and the positive rate of colonic p38MAPK protein expression in the model group increased (P<0.05, P<0.01), and the expression of p38MAPK was significantly correlated with IL- The levels of 1β, IL-6 and TNF-α were positively correlated.

　　Conclusion: The D-IBS rat model reconstructed by chronic restraint combined with senna gavage may increase the expression of p38MAPK and promote the release of IL-1β, IL-6 and TNF-α by activating the p38MAPK signaling pathway. Induce a low-grade inflammatory response in the intestinal mucosa.