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目的探讨脓毒症早期呼吸肌蛋白降解代谢变化的规律及机制。方法45只雄性Wistar大鼠随机分为烫伤组(B组)、脓毒症组(S组)及对照组(C组)。B组大鼠使用沸水致背部30%总体表面积Ⅲ度烫伤,S组大鼠以同样方法烫伤后,立即腹腔注射内毒素(6 mg/kg)制成烧伤脓毒症动物模型。分别于伤后2 h和6 h,采用高效液相-荧光法检测胸大肌、肋间肌和膈肌内三甲基组氨酸(3-MH)的含量,Northern杂交检测泛素、蛋白酶体C2亚基mRNA表达的变化。结果S组伤后2 h和6 h三处肌肉组织内3-MH的含量较B组和C组均显著升高(P<0.05),B组伤后2 h胸大肌和肋间肌内3-MH的含量较C组显著升高(P<0.05),伤后6 h三处肌肉组织内3-MH的含量均较C组显著升高(P<0.01)。S组伤后2 h和6h三处肌肉组织内泛素mRNA和蛋白酶体C2亚基mRNA表达较B组和C组均显著增强(P<0.01),B组伤后2 h和6 h三处肌肉组织内泛素和蛋白酶体C2亚基mRNA表达较C组均显著增强(P<0.05)。结论严重烫伤特别是合并内毒素攻击后早期,呼吸肌细胞泛素-蛋白酶体途径活性呈现持续增强现象,肌纤维蛋白降解率也显著增加。这对于进一步从蛋白降解角度探讨烧伤脓毒症时呼吸肌功能异常的机制有参考意义。
Objective To investigate the regularity and mechanism of respiratory muscle proteolytic metabolism in early sepsis. Methods Forty five male Wistar rats were randomly divided into burn group (B group), sepsis group (S group) and control group (C group). Rats in group B were scalded with 30% of the total surface area of the back for 3 degrees with boiling water. Immediately after burn in group S, endotoxin (6 mg / kg) was intraperitoneally injected into animal model of burn sepsis. The content of 3-methyl-histidine (3-MH) in pectoralis major muscle, intercostal muscle and diaphragmatic muscle was detected by HPLC-fluorescence method at 2 h and 6 h after injury respectively. The levels of ubiquitin, proteasome C2 subunit mRNA expression changes. Results The levels of 3-MH in muscle tissue in group S were significantly higher than those in group B and C at 2 h and 6 h after injury (P <0.05). In group B, the pectoralis major and intercostal muscles The content of 3-MH in muscle tissue in 3 groups at 6 h after injury was significantly higher than that in C group (P <0.01). The expression of ubiquitin mRNA and proteasome C2 subunit mRNA in S group were significantly increased at 3 h and 6 h after injury (P <0.01), and at 2 h and 6 h after injury in group B Ubiquitin and proteasome C2 subunit mRNA expression in muscle tissue were significantly increased (P <0.05). Conclusions Severe scalding, especially in the early stage of combined endotoxin challenge, the ubiquitin - proteasome pathway activity of respiratory muscle cells showed a continuous enhancement phenomenon, and the muscle fiber protein degradation rate was also significantly increased. This is of further significance for further exploring the mechanism of respiratory muscle dysfunction in burn sepsis from the viewpoint of protein degradation.