柴胡总多糖对内毒素血症大鼠肺损伤的影响

Effect of Total Polysaccharide of Bupleurum on Lung Injury in Endotoxemia Rats

目的:研究柴胡总多糖对脂多糖(LPS)诱导的内毒素血症(ETM)大鼠肺损伤的影响。方法:选取健康雄性清洁级SD大鼠40只,遵照随机数字表法,每组8只,共分为5组:对照组(生理盐水)、模型组(LPS)、地塞米松组(阳性药组)、柴胡总多糖低剂量组(LPS+柴胡总多糖低剂量)、柴胡总多糖高剂量组(LPS+柴胡总多糖高剂量)。尾静脉注射LPS (4 mg/kg)建立内毒素血症大鼠模型,1 h后分别灌胃给予柴胡总多糖(50 mg/kg、150 mg/kg),地塞米松(2 mg/kg)。测定对照组和模型组血液细菌内毒素含量。酶联免疫吸附试验(ELISA)法测定肺组织匀浆炎症因子[肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)]的水平。光镜和透射电镜下观察肺组织病理学变化。结果:模型组的血液细菌内毒素含量(EU/mL)明显高于对照组。与模型组相比,柴胡总多糖高剂量组可明显降低肺组织TNF-α、IL-1β和IL-6水平,减轻肺组织结构损伤。结论:柴胡总多糖通过抑制炎症反应,减轻LPS诱导的ETM大鼠肺损伤。

Objective:To study the effect of total polysaccharide of Bupleurum on lung injury induced by lipopolysaccharide(LPS)in rats with endotoxemia(ETM).Methods:Forty healthy clean male SD rats were selected and divided into 5 groups:control group(normal saline),model group(LPS),dexamethasone group(positive drug group),low dose group of bupleurum total polysaccharide(LPS+low dose of Bupleurum total polysaccharide),high dose group of bupleurum total polysaccharide(LPS+high dose of Bupleurum total polysaccharide).LPS(4 mg/kg)was injected into tail vein to establish endotoxemia rat model.After one hour,bupleurum polysaccharide(50 mg/kg,150 mg/kg)and dexamethasone(2 mg/kg)were given to rats respectively by gavage.The endotoxin content in blood of control group and model group was detected.The levels of inflammatory factors[tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),interleukin-6(IL-6)]in lung homogenate were detected by enzyme-linked immunosorbent assay(ELISA).The histopathological changes of lung were observed under light and transmission electron microscopy.Results:The level of bacterial endotoxin(EU/ml)in the model group was significantly higher than that in the control group.Compared with the model group,the high-dose group can significantly reduce the levels of TNF-α,IL-1βand IL-6 in lung tissue,and reduce the structural damage of lung tissue.Conclusion:Bupleurum total polysaccharide can reduce LPS-induced lung injury in ETM rats by inhibiting inflammatory response.