摘要
目的:观察细菌性腹膜炎致MODS大鼠小肠平滑肌细胞COX-2、NF-κB和HSP70蛋白的表达,以及大承气汤的干预作用及其机理。方法:健康成年Wistar大鼠100只,随机分为对照组、MODS模型组和DCQD治疗组。MODS模型组和DCQD治疗组大鼠腹腔注射E.coli混悬液,建立细菌性腹膜炎致MODS模型。造模24 h后取存活大鼠上段小肠组织,利用免疫组织化学方法检测COX-2、NF-κB和HSP70蛋白的表达。结果:DCQD治疗组胃肠扩张、梗阻较MODS组明显减轻。免疫组化显示,DCQD治疗组大鼠小肠肌层COX-2、NF-κB和HSP70蛋白的表达较MODS组明显降低,环层肌COX-2和HSP70蛋白表达的降低尤为明显。结论:DCQD可以通过抑制COX-2/NF-κB促炎信号通路,减轻平滑肌的应激损伤,促进胃肠动力的恢复。
Objective To observe the expression of cyclooxygenase-2 (COX-2), nuclear factor-kappa B (NF-κB), and heat shock proteinT0 (HSP70) proteins in small intestinal smooth muscle cells of rats with multi- ple organ dysfunction syndrome (MODS) induced by bacterial peritonitis, and the intervention effect of Da Cheng Qi Decoction (DCQD), and to discuss the mechanism of gastrointestinal motility disorders caused by MODS and DCQD treatment. Methods One hundred Wistar rats weighing 200 to 250 g were randomly divided into: con- trol group, MODS model group and DCQD treated group. The rats in MODS model group and DCQD treated group were injected of E.eoli suspension into abdominal cavity under sterile condition. The rats in DCQD treated group were administrated by gavage with DCQD two days before the suspension was injected. Twenty-four hours after injection, the proximal segment of intestine was tested by immunohistochemistry for analysis of COX-2. NF-κB and HSP70 proteins expression. Results Compared with the control group, integral optical density (IOD) values of COX-2, NF-κB and HSP70 proteins of small intestine in the MODS group were significantly in- creased (P 〈 0.01). Compared with the MODS group, IOD value of COX-2, NF-κB and HSP70 proteins in the DCQD group were significantly decreased (P 〈 0.01), especially COX-2 and HSP70 in circular smooth muscle. Conclusion DCQD can promote the recovery of gastrointestinal motility by inhibition of COX-2/NF-κB inflam- matory signaling pathway, and reduce stress injury of smooth muscle cells.
出处
《中国中西医结合外科杂志》
CAS
2012年第4期365-369,共5页
Chinese Journal of Surgery of Integrated Traditional and Western Medicine
基金
国家自然科学基金资助项目(30973852)
辽宁省高等学校科研项目计划资助项目(2008S074)