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目的探讨ANGPTL4免疫脂质体对转染脂多糖(lipopolysaccharide,LPS)诱发的急性肺损伤(acute lung injury,ALI)小鼠,肺损伤的影响。方法采用逆相蒸发法制备ANGPTL4基因表达质粒与抗CD31抗体偶联的免疫脂质体;LPS诱发急性肺损伤小鼠模型;观察经ANGPTL4免疫脂质体转染的急性肺损伤小鼠的肺部炎症因子肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-6(interleukin-6,IL-6)水平和中性粒细胞活化标志物髓过氧化物酶(myeloperoxidase,MPO)表达的变化,以及小鼠肺组织病理变化和肺血管通透性的改化。结果 ANGPTL4免疫脂质体可以有效增加小鼠肺内ANGPTL4的表达;进而降低ALI小鼠肺泡灌洗液中的TNF-α、IL-6水平和MPO的表达;降低ALI小鼠肺组织湿干比和肺泡灌洗液蛋白浓度,减轻肺组织病变程度。结论 ANGPTL4免疫脂质体能有效减轻LPS诱导的ALI小鼠的肺部炎症损伤反应。
Objective To investigate the effects of ANGPTL4 immunoliposomes on lung injury induced by lipopolysaccharide (LPS) -induced acute lung injury (ALI) in mice. Methods Anti-CD31 antibody-coupled immunosorbent plasmids (ANGPTL4) were prepared by reversed-phase evaporation method. A mouse model of acute lung injury induced by LPS was established. The lungs of mice with acute lung injury The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and neutrophil activation marker myeloperoxidase MPO) expression changes, as well as mouse lung tissue pathological changes and pulmonary vascular permeability changes. Results ANGPTL4 immunoliposomes could effectively increase the expression of ANGPTL4 in the lungs of mice, and then decrease the levels of TNF-α, IL-6 and MPO in the alveolar lavage fluid of ALI mice; And alveolar lavage fluid protein concentration, reduce lung tissue lesions. Conclusion ANGPTL4 immunized liposomes can effectively reduce the inflammatory response induced by LPS in lung of ALI mice.