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磷脂酶Ａ２可能通过以下途径参与急性肺损伤的发生过程：（１）直接分解肺组织生物膜磷脂和肺泡表面活性物质中的磷脂成份；（２）催化合成前列腺素、血小板激活因子、白三烯等脂类介质；（３）与体内其它炎症介质（如肿瘤坏死因子、白介素等）协同作用。从而破坏肺泡上皮、肺毛细血管内皮细胞的完整性，增加肺毛细血管的通透性和炎细胞浸润，增加肺泡表面张力，降低肺顺应性，引发肺水肿和呼吸功能障碍。而磷脂酶Ａ２抑制剂对多种原因引起的急性肺损伤具有一定的保护作用。
Phospholipase A2 may be involved in the pathogenesis of acute lung injury by (1) direct breakdown of phospholipid components in lung tissue biofilm phospholipids and alveolar surfactant; (2) catalytic synthesis of prostaglandins, platelet activating factor, leukotrienes And other lipid media; (3) and other inflammatory mediators in vivo (such as tumor necrosis factor, interleukin, etc.) Synergy. Thereby disrupting the integrity of the alveolar epithelium, pulmonary capillary endothelial cells, increasing pulmonary capillary permeability and inflammatory cell infiltration, increase alveolar surface tension, reduce lung compliance, trigger pulmonary edema and respiratory dysfunction. The phospholipase A2 inhibitor for a variety of causes of acute lung injury has a protective effect.