OBJECTIVE:To explore the protective effects of polysaccharide sulphate (PSS) on mice with acute lung injury.METHODS:The mice were randomized into control group,PSS group (10 mg/kg),model group (lipopolysaccharide 10 mg/kg)and treatment group (lipopolysaccharide 10 mg/kg+PSS 10 mg/kg) with 10 mice in each group.The mice were sacrificed 8 h after intravenous injection via tail; the pathological manifestation of lungs was observed under light microscope,and the wet/dry (W/D)weight ratio,intercellular adhesion molecular-1 (ICAM-1) and tumour necrosis factor-α (TNF-α) levels in lung tissue were calculated; the activity ofNF-κB p65 in the lung tissue was detected by immunohistochemistry method.RESULTS:The integration of pulmonary structure was observed in control group and PSS group,and no histological injury of lung was observed.Compared with control group,significant pathological injury and severe pulmonary edema were found,and the ICAM-1 and TNF-α levels and NF-κB p65 activity in lung tissue were increased significantly (P＜0.05) in model group and treatment group; and above index of PSS group had no statistical significance (P＞0.05).Compared with model group,above index of treatment group were improved significantly (P＜0.05).CONCLUSIONS:PSS can improve lipopolysaccharide-induced acute lung injury in mice significantly,which may be associated with the inhibition of NF-κB p65 activity.%目的:研究藻酸双酯钠(PSS)对急性肺损伤模型小鼠的保护作用.方法:将小鼠随机分为对照组、PSS(10 mg/kg)组、模型(脂多糖10 mg/kg)组、治疗(脂多糖10mg/kg+PSS 10mg/kg)组,每组10只.尾静脉注射相应药物8h后,处死,光镜下观察肺组织形态学变化,测定肺组织湿干质量比值(W/D)和肺组织中细胞间黏附因子1(ICAM-1)和肿瘤坏死因子α(TNF-α)的浓度,免疫组化法测定肺组织中核转录因子-κB (NF-κB)p65的活性.结果:对照组和PSS组小鼠肺组织结构完整,无肺组织病理损伤变化.与对照组比较,模型组和治疗组小鼠肺组织有明显病理学损伤,肺水肿严重,肺组织中ICAM-1、TNF-α浓度和NF-κBp65活性明显增加(P＜0.05),PSS组小鼠上述指标差异无统计学意义(P＞0.05).与模型组比较,治疗组小鼠上述指标均明显改善(P＜0.05).结论:PSS能明显改善脂多糖诱导的小鼠急性肺损伤,其机制可能与抑制NF-κBp65活性有关.
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