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目的:研究抗肿瘤坏死因子α抗体(anti-TNF-αantibody)对腹部创伤合并感染脓毒血症大鼠的急性胰岛素抵抗的影响机制。方法:建立大鼠创伤脓毒症导致高血糖的动物模型,并随机分为4组,分别给予大剂量和小剂量抗TNF-α治疗;通过血糖、血清胰岛素水平、葡萄糖耐量试验以及高胰岛素正葡萄糖钳夹试验等方法比较各组大鼠的差异。结果:采用抗TNF-α抗体治疗可显著降低术后血清胰岛素水平、葡萄糖耐量、葡萄糖输注率和肝组织Akt磷酸化水平,提高mTOR磷酸化水平。结论:抗TNF-α抗体治疗可调节肝组织胰岛素信号通路Akt和mTOR的磷酸化水平,进而减轻创伤感染应激后大鼠急性胰岛素抵抗程度。
Objective: To investigate the mechanism of anti-TNF-α antibody on acute insulin resistance in septic rats with abdominal trauma complicated with sepsis. Methods: Animal models of sepsis-induced hyperglycemia in rats were established and randomly divided into 4 groups: high-dose and low-dose anti-TNF-α treatment. The blood glucose, serum insulin level, glucose tolerance test and hyperinsulinism Glucose clamp test and other methods to compare the differences in rats. Results: Anti-TNF-α antibody treatment could significantly reduce postoperative serum insulin levels, glucose tolerance, glucose infusion rates and liver Akt phosphorylation levels, increased mTOR phosphorylation. Conclusion: The anti-TNF-α antibody can regulate the phosphorylation of Akt and mTOR in hepatic tissue, and then reduce the degree of acute insulin resistance in trauma-infected rats.