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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 lung injury induced by endotoxin in rats. Methods Thirty - six Wistar rats were randomly divided into saline control group, lipopolysaccharides (LPS) group and LPS + U74006F group, 12 rats in each group. The wet and dry ratio of lung tissue was calculated to analyze the edema of lung tissue in each group. HE staining and immunohistochemical staining of paraffin embedded in lung tissue were performed to detect the expression of inflammatory cytokines in serum and bronchoalveolar lavage fluid. Results The expression of MDA and HNE, IL-1β and TNF-α in serum, BALF and lung homogenate of endotoxin-induced lung injury model were significantly increased, the difference was statistically significant (P <0.05). The level of MDA, HNE, inflammatory cytokines IL-1β and TNF-α decreased after UFA inhibitor U74006F was applied. The difference was statistically significant (P <0.05). Conclusion Endotoxin can obviously induce lung injury in rats, and lipid peroxidation can significantly aggravate the degree of lung injury.