中文摘要：

目的探讨c-Jun氨基末端激酶（c-JunNH（2）-terminal kinase，JNK）在烧伤后胰岛素抵抗中的作用及其机制。方法将24只SD大鼠随机分为对照组、烧伤组和烧伤＋anisomycin组。烧伤组和烧伤＋anisomycin组大鼠制成30％总体表面积（TBSA）三度烧伤模型。烧伤＋anisomycin组大鼠伤后第4天静脉注射anisomycin[5mg／kg，溶于250-二甲基亚砜（DMSO）]，其余两组静脉注射250μl DMSO，2h后进行正常血糖高胰岛素钳夹技术实验，然后采集肌肉标本，采用免疫沉淀和免疫印迹观测肌肉组织胰岛素受体底物1丝氨酸307（IRS-1 Ser307）磷酸化和酪氨酸活性变化并观察肌肉组织磷酸化JNK的差异。结果正常血糖高胰岛素钳夹技术实验中对照组、烧伤组和烧伤＋anisomycin组10％葡萄糖输注率（mg·kg^-1·min^-1）分别为12．3±0．4，6．6±0．3，6．5±0．4。烧伤后肌肉组织IRS-1磷酸化丝氨酸307活性明显升高，而IRS-1磷酸化酪氨酸活性明显降低，磷酸化JNK活性升高。结论JNK通过增加烧伤大鼠IRS-1磷酸化丝氨酸307活性，至少部分参与了烧伤后胰岛素抵抗。

英文摘要：

Objective To investigate the role of c-Jun NH（2）-terminal kinase （JNk） in insulin resistance after burn and its mechanism. Methods Twenty-four Sprague-Dawley rats were randomized to control, burn and burn ＋ anisomycin groups. The rats in control group received sham burn trauma, and burn and burn ＋ anisomycin groups received 30% total bady surface area （TBSA） full thickness burn injury. Anisomycin （5 mg/kg） together with 250 μl dimethyl sulfoxide （DMSO） was injected to the rats in anisomycin group intravenously, and only 250 μl DMSO in the other two groups. Euglycemichyperinsnlinemic glucose clamps was performed 2 hours after the injection. The changes of phospho-serine 307, phuspho-tyrosine of insulin receptor substrale （IRS）-1 and phuspho-JNK in muscle tissues were determined and compared using immunoprecipitation and Western blot analysis or immunohistochemistry in the three groups. Results The infusing rates of total 10% glucose （ mg · kg^-1 · min^-1 ） in control, burn and burn ＋ anisomycin group were 12.3 ± 0. 4, 6. 6 ± 0. 3, 6. 5 ± 0. 4, respectively. The level of IRS-1 Serine307 phusphorylation and phospho-JNK in muscle increased significantly, while insulin-induced tyrosine phusphorylation of IRS-1 decreased markedly after burn. Conclusions The activation of JNK elevates the level of IRS-1 phuspho-serine 307 and might play a role in insulin resistance after burn in rats.