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目的探讨 c-Jun 氨基末端激酶(c-Jun NH(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[5 mg/kg,溶于250μl二甲基亚砜(DMSO)],其余两组静脉注射250μl DMSO,2 h 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。
Objective To investigate the role and mechanism of c-Jun N-terminal kinase (c-Jun NH (2) -terminal kinase, JNK) in postburn insulin resistance. Methods Twenty-four SD rats were randomly divided into control group, burn group and burn + anisomycin group. The burn group and the burn + anisomycin group were made into the third burn model with 30% total surface area (TBSA). The rats in burn + anisomycin group were intravenously injected with anisomycin [5 mg / kg dissolved in 250 μl dimethylsulfoxide (DMSO)] on the 4th day after injury, and the other two groups were injected with 250 μl DMSO intravenously. After 2 hours, Then the muscle samples were collected and the phosphorylation and tyrosine activities of serine 307 (IRS-1 Ser307) in muscle tissue were detected by immunoprecipitation and immunoblotting. The differences of phosphorylated JNK in muscle tissue were observed. Results In normal high glucose hyperinsulinemic clamp technique, 10% glucose infusion rate (mg · kg -1 · min -1) in the burn group and the burn + anisomycin group was 12.3 ± 0.4,6.6 ± 0.3, 6.5 ± 0.4. After burn, IRS-1 phosphorylation serine 307 activity was significantly increased, but IRS-1 phosphorylation tyrosine activity was significantly decreased, phosphorylated JNK activity increased. Conclusion JNK at least partially participates in insulin resistance after burn injury by increasing IRS-1 phosphorylation serine 307 activity in burn rats.