Ulinastain with ghrelin improves small intestine dysfunction in endotoxemia rats / 局解手术学杂志

ABSTRACT

Objective To evaluate the antiinflammatory effect of ulinastain( UTI) with ghrelin( GHL) on amelioration of small intestine dysfunction and its possible mechanisms in endotoxemia rats. Methods Animals were received intraperitoneal injection with lipopolysaccha-ride(LPS,15 mg/kg)as a endotoxemia model. 60 male SD rats were randomly divided into control group(CON group),LPS group,UTI group,GHL group,and UTI+GHL group. Microstructure of small intestinal submucosa was observed with HE staining. Dextran blue-2000 (BD-2000)was drenched for calculation of propulsion rate of the small intestine. The level of tumor necrosis factorα(TNF-α),IL-6 and HMGB1 in serum and small Intestinal mucosal tissue were determined by enzyme linked immunosorbent assay( ELISA) . RealTime-PCR was administrated for detection of rat defensin-5 mRNA(RD-5)and trefoil factor family-3(TFF-3)mRNA. All above measurement were taken re-spectively at 12 hours and 24 hours after LPS injection. Results HE staining shows that UTI+GHL group significantly alleviate the damage of intestinal microtructure caused by LPS when compared with UTI group and GHL group. The UTI+GHL group markedly increased expres-sion of RD-5 and TFF3 mRNA than those of UTI and GHL group in small Intestinal mucosal tissue (P<0. 05). Both the GHL group and the UTI+GHL group significantly enhanced the function of intestine motility,but the propulsion rate of UTI+GHL group was significant higher than that of GHL group(P<0. 05). In LPS group,the level of TNF-α、IL-6 and HMGB1 both in serum and intestinal mucosa tissue were markedly increased(P<0. 05),but those of UTI group,GHL group and UTI+GHL group were significantly decreased when compare to LPS group after the drugs administration at 12 and 24 hours. Conclusion UTI combined with GHL can significantly improve the intestinal func-tion of mucosal barrier and the motor through the inhibition of both systemic and intestinal mucosal inflammatory reaction in the process of en-dotoxemia.