摘要
目的探讨脂质过氧化反应对内毒素诱导大鼠肺损伤的作用。方法 36只Wistar大鼠随机分为生理盐水对照组、脂多糖(lipopolysaccharides,LPS)处理组、LPS处理+U74006F组,各12例。计算肺组织干湿比分析各组肺组织水肿的情况,肺组织石蜡包埋行HE染色和免疫组化,检测血清和肺泡灌洗液炎性因子表达。结果内毒素诱导肺损伤模型中的血清、肺泡灌洗液和肺组织匀浆,脂质过氧化产物MDA和HNE、炎症因子IL-1β和TNF-α的表达都明显增加,差异有统计学意义(P<0.05)。当应用脂质过氧化抑制剂U74006F后,可减轻肺组织损伤的程度,表现为MDA、HNE、炎症因子IL-1β和TNF-α的表达下降,差异有统计学意义(P<0.05)。结论内毒素可明显诱导大鼠的肺损伤,而脂质过氧化可明显加重肺损伤的程度。
Objective To investigate the effect of lipid peroxidation on rat with lung injury induced by endotoxin. Meth-ods 36 Wistar rats were randomly divided into normal saline control group,lipopolysaccharide （ lipopolysaccharides,LPS） treat-ment group,LPS＋U74006F treatment group,each of 12 cases. The pulmonary tissue edema in the lung tissue was calculated and the lung tissue was paraffin embedded,HE stained and immunohistochemistry. The expression of inflammatory factors in serum and bronchoalveolar lavage fluid was detected. Results The lipid peroxidation product MDA and HNE,inflammatory cytokines IL-1 and TNF -mRNA expression in serum,bronchoalveolar lavage fluid and lung tissue homogenate of lung injury model induced by endotoxin were all significantly increased,and the difference was statistically significant（P〈0. 05）. After the application of lipid peroxidation inhibitor U74006F,the degree of lung tissue injury could be reduced,the expression of MDA,HNE,the expression of inflammatory factor IL-1 beta and TNF-alpha decreased,and the difference was statistically significant（P〈0. 05）. Conclusion Endotoxin can obviously induce lung injury in rats,and lipid peroxidation can obviously increase the degree of lung injury.
出处
《四川医学》
CAS
2016年第8期840-844,共5页
Sichuan Medical Journal
基金
四川省医学科研青年创新课题基金(编号:Q15052)
关键词
内毒素
肺损伤
脂多糖
脂质过氧化反应
氧化应激
endotoxin
lung injury
lipopolysaccharide
lipid peroxidation
oxidative stress
