Effect of early fluid resuscitation combined with low dose cyclophosphamide on intestinal barrier function in severe sepsis rats.

Abstract

To investigate the effect of early fluid resuscitation on intestinal microecology in rats with severe sepsis. The severe sepsis model used was mainly cecal ligation perforation (CLP) model. Male SD rats were randomly divided into five groups: sham, CLP, CLP + normal saline (NS), CLP + cyclophosphamide (CTX), and CLP + NS + CTX. (1) The levels of IL-6, IL-10, and TNF-α in peripheral blood were measured by ELISA. (2) The expression of occludin/β-action in colonic tissue of mice was examined by Western Blot. (3) The intestinal permeability was measured by FD70 detection. (4) The length of the chorionic membrane was measured by colon histopathological staining. (5) The intestinal epithelial cell apoptosis was measured with the apoptosis index. (1) The rat model of severe sepsis was successfully replicated, and the 7-day survival rate of sepsis mice in each group was analyzed. (2) The expression level of splenic junction protein and the pathological damage in colonic tissue of the severe sepsis mice was significantly different between sham, CLP, CTX, NS, and NS + CTX (P < 0.05). The expression of tight junction protein in the NS + CTX mice was the highest, and the pathological damage was the smallest. (3) The colonic tissue apoptosis and intestinal permeability in the severe sepsis mice were compared with those of the colon tissues (P < 0.05). (4) The expression levels of IL-6, IL-10, and TNF-α in peripheral blood were significantly increased after severe sepsis (P < 0.01). The expression of IL-6 and TNF-alpha in each treatment group decreased (P < 0.05), while the expression of IL-10 in NS + CTX group increased significantly (P < 0.01). (1) We successfully replicated the rat model of severe sepsis. (2) Early fluid intervention and cyclophosphamide treatment can significantly improve the 7-day survival rate of the sepsis mice. (3) The fluid resuscitation and cyclophosphamide can delay intestinal damage to the intestinal tract barrier function and play a protective role.