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目的观察丙酮酸乙酯(ethyl pyruvate,EP)对烫伤大鼠肺组织高迁移率族蛋白B1(high mobility group box-1protein,HMGB1)表达水平及急性肺损伤的影响。方法采用大鼠30%总体表面积Ⅲ度烫伤延迟复苏模型,78只雄性Wistar大鼠按随机数字表法分为假烫伤组(n=18)、烫伤组(n=30)、EP治疗组(n=30),每组分别在假伤或伤后第8、24、72小时活杀留取肺组织。HMGB1基因/蛋白表达分别采用逆转录聚合酶链反应及蛋白免疫印记法、免疫组化方法检测;髓过氧化物酶(myelope roxidase,MPO)活性采用酶学分光光度法测定;并采用HE染色、光镜下观察肺组织病理改变。结果与假烫伤组比较,烫伤组肺组织HMGB1基因/蛋白表达于伤后8～72h显著增强(P<0.05,P<0.01),同时肺组织MPO活性在8h及24h明显升高(P<0.01),病理学观察见肺组织炎细胞浸润,正常结构破坏,其中以24h改变最重。与烫伤组比较,EP治疗组大鼠肺组织8～72h时间点HMGB1表达显著下调(P<0.05),肺组织MPO活性在8、24h时间点显著下降(P<0.01),EP治疗组8～72h肺组织病理形态损害明显减轻。结论HMGB1作为晚期炎症因子参与了烫伤后肺组织炎症反应的病理过程,EP治疗可明显下调肺组织HMGB1表达,并有助于降低肺组织MPO活性,从而减轻烫伤延迟复苏所致急性肺损伤。
Objective To observe the effect of ethyl pyruvate (EP) on the expression of high mobility group box-1 protein (HMGB1) and acute lung injury in scalded rats. Methods The model of delayed resuscitation with burn degree of 30% of the total surface area of rats was adopted. 78 male Wistar rats were randomly divided into sham burn group (n = 18), burn group (n = 30), EP group = 30). The lungs were sacrificed on the 8th, 24th and 72th hour after the injury or injury. The expression of HMGB1 gene / protein was detected by reverse transcriptase polymerase chain reaction (RT-PCR), Western blot and immunohistochemistry respectively. The activity of myeloperoxidase (MPO) was measured by enzymolysis spectrophotometry. HE staining, Lung tissue pathological changes were observed under light microscope. Results Compared with fake scalded group, the expression of HMGB1 gene and protein in lung tissue of scalded group increased significantly (P <0.05, P <0.01) at 8h to 72h after injury, while MPO activity in lung tissue increased significantly at 8h and 24h (P <0.01) ), Pathological observation of inflammatory cell infiltration of lung tissue, the normal structure damage, of which the most severe changes in 24h. Compared with scald group, the expression of HMGB1 in lung tissue of EP group was significantly decreased at 8h to 72h (P <0.05), the MPO activity in lung tissue decreased significantly at 8h and 24h (P <0.01) 72h lung tissue pathological damage was significantly reduced. Conclusion HMGB1 is a late inflammatory cytokine involved in the pathological process of inflammatory reaction in lung tissue after scald. EP treatment can significantly down-regulate the expression of HMGB1 in lung tissue and decrease the activity of MPO in lung tissue, thus reducing the acute lung injury induced by delayed resuscitation.