血必净对脂多糖诱导的急性肺损伤大鼠肺组织高迁移率族蛋白1表达的影响

The effect of Xuebijing on expression of HMGB1 in lipopolysaccharide-induced acute lung injury in rats

目的观察脂多糖诱导的急性肺损伤(ALI)大鼠HMGB1的表达及应用血必净的干预效果,并探讨作用机制。方法 45只W istar大鼠随机分为三组:(1)健康对照(Control)组(15只)、(2)脂多糖(LPS)组(15只)、(3)血必净干预(XBJ)组(15只)。LPS组和XB J组采用股静脉注射LPS(5mg/kg)建立大鼠ALI模型。造模前半小时开始给药,XBJ组给予血必净4 m l/kg,静脉注射;Control组和LPS组则给予等容积0.9%氯化钠注射液。在造模后6 h、12 h、24 h各随机处死大鼠5只,分别作为I、II、Ⅲ亚组,光镜下观察肺脏组织形态学变化,免疫组织化学法(IHC)检测肺组织中HMGB1蛋白表达。结果造模后LPS组随着实验时间的延长,肺组织HMGB1蛋白呈逐渐增加趋势,至24 h达到高峰。与LPS组相比,血必净组各时间点肺组织HMGB1蛋白表达明显降低(P<0.05)。光镜显示LPS组肺组织病理形态学改变明显,而血必净组则明显减轻。结论血必净可明显抑制脂多糖诱导的急性肺损伤大鼠肺组织增强的HMGB1表达,减轻脂多糖诱导的大鼠肺损伤程度。

Objective To study high mobility group box 1（HMGB1）expression in lipopolysaccharide-induced acute lung injury in rats and investigate the effect of Xuebijing and its possible mechanism.Methods 45 Wistar rats were randomly divided into 3 groups as following：（1）control group（n=15）,（2）LPS group（n=15）,（3）Xuebijing treatment（XBJ）group（n=15）.LPS（5mg/kg）was infused by femoral vein to reproduce ALI model in LPS group and XBJ group.Male Wistar rats were given either saline in LPS group or XBJ in XBJ group 4ml/kg 30 min before the intravenous injection of a bolus of LPS,whereas control group were given equivalent volume normal saline.Five rats in each group were killed at 6h,12 h and 24 h,which were divided into subgroup I,Ⅱ,Ⅲ,and lung tissue was collected.The pathomorphism changes of lung tissue were observed using light microscope.and the expression of HMGB1 protein in pulmonary was examined by immunohistochemistry in all the rats.Results The expression of HMGB1 protein in pulmonary showed a gradual increase and reached the peak at 24h in LPS group.Lower level of HMGB1 protein was found in XBJ group than that in LPS group at all time points（P〈0.05）.The pathological change was more obvious in LPS group than that in XBJ group.Conclusion HMGB1 expression is increased in acute lung injury in the rats induced by LPS.Xuebijing could attenuate the degree of acute lung injury in rats induced by LPS,which may be related to its inhibition of the HMGB1 protein expression in lung tissue.