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目的:探讨δ阿片受体激动剂DADLE(D-Ala2-D-Leu5-enkephali)对脓毒症大鼠小肠屏障功能的保护作用及其机制。方法:72只SD大鼠,分为假手术组、脓毒症组和DADLE(5mg/Kg)治疗组,每组24只。采用改良盲肠结扎穿孔方法(CLP)建立大鼠脓毒症模型,假手术组除不结扎刺穿盲肠外,其余操作同脓毒症组,DADLE治疗组模型建立后立即按5mL/kg剂量静脉注射浓度为0.5mg/mL的DALDE。于手术后4、8、12h处死大鼠,测定小肠黏膜组织中ATP、ADP、AMP含量;制备肠上皮细胞线粒体,测定各组大鼠线粒体呼吸控制率(RCR)、磷氧比(P/O)和肠道氧摄取率(Oext);观察并比较各组小肠黏膜上皮组织病理改变。结果:DADLE治疗组的小肠黏膜ATP、ADP含量较脓毒症组均有明显升高(P<0.05),AMP含量明显下降(P<0.05);DADLE治疗组小肠上皮细胞中线粒体RCR、P/O和Oext较脓毒症组均明显升高(P<0.05);小肠黏膜上皮组织病理学提示DADLE组的组织损伤明显轻于脓毒症组。结论:δ阿片受体激动剂DADLE对脓毒症大鼠小肠氧代谢和能量代谢的抑制状态具有一定程度的改善作用。
Objective: To investigate the protective effect of δ-opioid receptor agonist DADLE (D-Ala2-D-Leu5-enkephali) on intestinal barrier function in septic rats and its mechanism. Methods: Seventy-two SD rats were divided into sham operation group, sepsis group and DADLE (5mg / Kg) treatment group, 24 rats in each group. The model of sepsis was established by modified cecal ligation and puncture (CLP). The rats in the sham operation group were treated with sepsis without ligating the cecum, and the rats in the DADLE treatment group were injected intravenously 5 mL / kg DALDE at a concentration of 0.5 mg / mL. The rats were sacrificed at 4, 8 and 12 h after operation to measure the content of ATP, ADP and AMP in intestinal mucosa. The mitochondria of intestinal epithelial cells were prepared and the mitochondrial respiratory control rate (RCR), P / O ratio ) And intestinal oxygen uptake rate (Oext); observed and compared the pathological changes of intestinal mucosal epithelium in each group. Results: Compared with the sepsis group, the content of ATP and ADP in the intestinal mucosa of DADLE treatment group was significantly increased (P <0.05) and AMP content was significantly decreased (P <0.05). The mitochondrial RCR and P / O and Oext were significantly higher than those in sepsis group (P <0.05). The histopathology of small intestinal mucosa epithelium suggested that the tissue injury in DADLE group was lighter than that in sepsis group. CONCLUSION: The δ opioid receptor agonist DADLE has a certain degree of improvement on the inhibition of intestinal oxygen metabolism and energy metabolism in septic rats.