中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2011年
2期
233-235
,共3页
乌司他丁%细菌性腹膜炎%小肠%NF-κB%一氧化氮
烏司他丁%細菌性腹膜炎%小腸%NF-κB%一氧化氮
오사타정%세균성복막염%소장%NF-κB%일양화담
Ulinastatin%Bacterial peritonitis%Intestinal%NF-κB%Nitric oxide
目的 探讨乌司他丁对细菌性腹膜炎大鼠小肠运动功能的保护作用及其机制.方法 将Wistar大鼠60只随机分成对照组、模型组和乌司他丁组.模型组和乌司他丁组制作细菌性腹膜炎动物模型,乌司他丁组于制模后30min静脉给予乌司他丁5万U/kg,其余组静脉给予等量生理盐水.观测各组大鼠小肠传输功能、小肠环行平滑肌条收缩能力、环行平滑肌细胞收缩反应及细胞内钙离子浓度([Ca2+]i)的变化;测定小肠平滑肌细胞核转录因子-κB(NF-κB)的活性;测定小肠肌层诱导型一氧化氮合酶(iNOS)mRNA的表达量和平滑肌细胞培养基中一氧化氮(NO)含量的变化.结果 乌司他丁组较模型组大鼠小肠传输明显改善.乙酰胆碱作用下,模型组和乌司他丁组小肠环行肌条收缩力分别为(0.75±0.06)、(1.87±0.29)g/mm2·s-1;平滑肌细胞收缩反应为(11.42±4.23)%、(37.22±10.08)%;[Ca2+]i变化为(119±21)%、(205±49)%.模型组和乌司他丁组小肠肌层iNOS mRNA表达水平分别为1.38±0.41、0.58±0.17;平滑肌细胞培养基NO浓度为(98.34±19.62)、(32.72±7.98)μmol/L;平滑肌细胞NF-κB活性为303.25±47.18、170.22±29.62.结论 乌司他丁通过抑制小肠肌层NF-κB蛋白的活化,下调细菌性腹膜炎大鼠小肠肌层iNOS mRNA的表达,保护小肠的运动功能.
目的 探討烏司他丁對細菌性腹膜炎大鼠小腸運動功能的保護作用及其機製.方法 將Wistar大鼠60隻隨機分成對照組、模型組和烏司他丁組.模型組和烏司他丁組製作細菌性腹膜炎動物模型,烏司他丁組于製模後30min靜脈給予烏司他丁5萬U/kg,其餘組靜脈給予等量生理鹽水.觀測各組大鼠小腸傳輸功能、小腸環行平滑肌條收縮能力、環行平滑肌細胞收縮反應及細胞內鈣離子濃度([Ca2+]i)的變化;測定小腸平滑肌細胞覈轉錄因子-κB(NF-κB)的活性;測定小腸肌層誘導型一氧化氮閤酶(iNOS)mRNA的錶達量和平滑肌細胞培養基中一氧化氮(NO)含量的變化.結果 烏司他丁組較模型組大鼠小腸傳輸明顯改善.乙酰膽堿作用下,模型組和烏司他丁組小腸環行肌條收縮力分彆為(0.75±0.06)、(1.87±0.29)g/mm2·s-1;平滑肌細胞收縮反應為(11.42±4.23)%、(37.22±10.08)%;[Ca2+]i變化為(119±21)%、(205±49)%.模型組和烏司他丁組小腸肌層iNOS mRNA錶達水平分彆為1.38±0.41、0.58±0.17;平滑肌細胞培養基NO濃度為(98.34±19.62)、(32.72±7.98)μmol/L;平滑肌細胞NF-κB活性為303.25±47.18、170.22±29.62.結論 烏司他丁通過抑製小腸肌層NF-κB蛋白的活化,下調細菌性腹膜炎大鼠小腸肌層iNOS mRNA的錶達,保護小腸的運動功能.
목적 탐토오사타정대세균성복막염대서소장운동공능적보호작용급기궤제.방법 장Wistar대서60지수궤분성대조조、모형조화오사타정조.모형조화오사타정조제작세균성복막염동물모형,오사타정조우제모후30min정맥급여오사타정5만U/kg,기여조정맥급여등량생리염수.관측각조대서소장전수공능、소장배행평활기조수축능력、배행평활기세포수축반응급세포내개리자농도([Ca2+]i)적변화;측정소장평활기세포핵전록인자-κB(NF-κB)적활성;측정소장기층유도형일양화담합매(iNOS)mRNA적표체량화평활기세포배양기중일양화담(NO)함량적변화.결과 오사타정조교모형조대서소장전수명현개선.을선담감작용하,모형조화오사타정조소장배행기조수축력분별위(0.75±0.06)、(1.87±0.29)g/mm2·s-1;평활기세포수축반응위(11.42±4.23)%、(37.22±10.08)%;[Ca2+]i변화위(119±21)%、(205±49)%.모형조화오사타정조소장기층iNOS mRNA표체수평분별위1.38±0.41、0.58±0.17;평활기세포배양기NO농도위(98.34±19.62)、(32.72±7.98)μmol/L;평활기세포NF-κB활성위303.25±47.18、170.22±29.62.결론 오사타정통과억제소장기층NF-κB단백적활화,하조세균성복막염대서소장기층iNOS mRNA적표체,보호소장적운동공능.
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.
