Lin Meng-Chih, Leung Sum Yee, Fang Wen-Feng, Chin Chien-Hung, Chung Kian Fan
Division of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Chang Gung Med J. 2010 Sep-Oct;33(5):501-8.
Diaphragmatic muscle impairment is an important cause of respiratory failure during sepsis. Insulin-like growth factor I (IGF-I) is an anabolic growth factor which prevents muscle degradation and wasting during sepsis, but its role in the diaphragmatic muscle during sepsis is unknown. The aim of this study was to investigate the expression of IGF-I in the diaphragmatic muscle in a murine model of sepsis induced by lipopolysaccharide (LPS).
Male B57 mice were peritoneally injected with LPS, and were killed and studied at different time-points, 24 h, 48 h, 72 h, and 96 h after injection. Diaphragm sarcolemmal damage was visualized by orange tracer dye infusion, and the expression of IGF-I, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in diaphragm tissue extracts were measured using ELISA.
LPS induced sarcolemmal damage in diaphragm myofibers from 24 h to 96 h, which was accompanied by a significant increase in IL-1β expression in the tissues while IGF-I levels were down-regulated. No change in TNF-α was observed. Body weights of animals were also reduced, especially at 96 h.
The expression of IGF-I in diaphragm tissues was down-regulated during sepsis- induced diaphragm myofiber damage, suggesting that IGF-I may be an important factor in the regulation of diaphragm myofiber repair. Further studies are needed to examine the mechanisms involved.
膈肌功能障碍是脓毒症期间呼吸衰竭的重要原因。胰岛素样生长因子I（IGF-I）是一种合成代谢生长因子，可防止脓毒症期间肌肉降解和消瘦，但其在脓毒症期间膈肌中的作用尚不清楚。本研究旨在探讨脂多糖（LPS）诱导的脓毒症小鼠模型中膈肌中IGF-I的表达。
雄性B57小鼠腹腔注射LPS，并在注射后24小时、48小时、72小时和96小时的不同时间点处死并进行研究。通过橙色示踪染料注入观察膈肌肌膜损伤，并使用ELISA测量膈肌组织提取物中IGF-I、白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）的表达。
LPS在24小时至96小时期间诱导膈肌肌纤维的肌膜损伤，同时组织中IL-1β表达显著增加，而IGF-I水平下调。未观察到TNF-α的变化。动物体重也有所下降，尤其是在96小时时。
脓毒症诱导的膈肌肌纤维损伤期间，膈肌组织中IGF-I的表达下调，提示IGF-I可能是调节膈肌肌纤维修复的重要因素。需要进一步研究以探讨其中涉及的机制。
