Abstract

Objective To explore the Protective effect and the mechanism of Ulinastatin (UTI) on intestinal motility in rats with bacterial peritonitis. Methods Sixty Wistar rats were divided randomly into control group, model group and UTI group (n=20 each), and the latter two groups were used to replicate bacterial peritonitis model. Rats in UTI group received UTI injection (50 000 U/kg) via tail vein, while rats in other groups were given equal volume saline. Gut transits in vivo and intestinal circular muscle contractions were measured in an organ bath. The contractile response of dispersed circular smooth muscle cells and the changes of[Ca2+]1 stimulated by aceylcholine were observed. Nuclear factor-κB (NF-κB) activity was examined by using electrophoretic mobility shift assay (EMSA). Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of inducible nitric oxide synthase (iNOS) mRNA within intestinal muscularis, and the level of nitric oxide (NO) in cell cultures was quantified. Results The gut transits in UTI group were improved obviously as compared with model group. In model group and UTI group, circular smooth muscle contractility stimulated by aceylcholine was (0. 75 ±0. 06 ) g/mm2· s - 1 and ( 1.87 ± O. 29 ) g/mm2· s - 1; contractile response of dispersed circular smooth muscle cells was ( 11.42 ± 4. 23 ) % and ( 37.22 ± 10. 08 ) %; changes of[Ca2+]1 was ( 119 ± 21 ) % and (205 ±49)%. In model group and UTI group, the activity of NF-κB was 303.25 ±47.18 and 170. 22 ±29.62; levels of iNOS mRNA expression were 1.38 ±0. 41 and 0. 58 ±0. 17; NO production was (98. 34± 19. 62) μmol/L and (32. 72 ±7.98) μmol/L respectively. Conclusion UTI has the ability to protect the intestinal motility in rats with bacterial peritonitis through inhibiting the activity of NF-κB and down-regulating the expression of iNOS mRNA within intestinal muscularis. Key words: Ulinastatin; Bacterial peritonitis; Intestinal; NF-κB; Nitric oxide

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