【摘要】 目的探讨HMGB1-TLR4-MyD88-NF-κB信号通路在胸部创伤多发肋骨骨折后心肌损伤的调节机制,观察心肌损伤后炎性细胞因子IL-4、 IL-6、IL-10表达变化。方法 (1)根据自由落体原理自制大鼠胸部创伤后多发肋骨骨折伴心肌损伤的模型;(2)实验分组:①对照组;②创伤后4 h组、创伤后8 h组、创伤后12 h组;各组雄性大鼠10只。检测各组心肌组织TLR4、MyD88、NF-κBp65、P-NF-κBp65蛋白含量;检测血浆心肌损伤标志物肌钙蛋白I(cTnI)、HMGB1、IL-4、IL-6、IL-10水平变化。结果与对照组比较,创伤后4 h心肌组织TLR4、MyD88、P-NF-κBp65即开始上升;创伤后随时间延长表达明显增高(P <0.05),NF-κBp65无明显的变化;血浆TnI、HMGB1、IL-6水平与对照组比较,创伤后4 h即开始上升;且随时间延长表达明显增强(P <0.05),但IL-4、IL-10无明显的上升。结论内源性危险分子HMGB1于胸部创伤后明显表达上升,激活TLR4-MyD88-NF-κB信号通路,同时刺激前炎症细胞因子IL-6等大量释放,加重心肌损伤。更多还原

【Abstract】 Objective To explore the regulatory mechanism of HMGB1-TLR4-MyD88-NF-κB signaling pathway in the myocardial injury following multiple rib fractures after chest trauma, and to observe the changes in the expressions of inflammatory cytokines IL-4, IL-6 and IL-10 after myocardial injury.Methods The model of multiple rib fractures with myocardial injury after chest trauma in rats was established based on the Law of Free Fall. Forty rats were selected. They were divided into control group, 4 h after trauma group, 8 h after trauma group and 12 h after trauma group with ten male rats in each group. The contents of TLR4, MyD88, NF-κBp65, P-NF-κBp65 were detected. Moreover, serum levels of cTnI, HMGB1, IL-4, IL-6, IL-10 markers of myocardial injury were detected in each group. Results Compared with the control group,TLR4, MyD88 and NF-κBp65 started to increase after 4 hours the trauma. The expression was significantly increased with time after the trauma(P <0.05).Plasma levels of TnI,HMGB1 and IL-6 began to rise 4 hours after the trauma compared with the control group.The expression significantly increased with time(P <0.05), but IL-4 and IL-10 did not increase significantly. Conclusion The expression of endogenous danger signal HMGB1 increased significantly after chest trauma, activating the TLR4-MyD88-NF-κB signaling pathway and simultaneously stimulating the release of a large number of inflammatory cytokines such as IL-6, which aggravates myocardial injury.更多还原