丹参酮对海水淹溺性肺损伤的保护机制研究

The pathogenesis of Tanshinone Ⅱ A protects seawater aspiration - induced lung injury

目的 观察海水淹溺性肺损伤的发病机制,验证丹参酮可以通过抑制巨噬细胞迁移抑制因子（MIF）减轻淹溺肺损伤.方法 24只大鼠分为正常对照组、海水淹溺组和丹参酮组.海水淹溺组气管内注入4 mL/kg海水,丹参酮组在造模后30 min腹腔内注入丹参酮（25 mg/kg）,4 h检测PaO2及肺损伤指标,并用RT-PCR和Western blot法检测MIF的转录及合成.结果 相对于正常对照组,海水淹溺组大鼠出现肺水肿,低氧血症,并伴有肺组织中性粒细胞的聚集及通透性增加,同时肺组织内MIF高表达,髓过氧化酶（MPO）活性随之增高.丹参酮干预后肺损伤减轻,MIF的高表达受到抑制,并伴随MPO活性降低.结论 MIF的促炎机制参与了淹溺肺损伤的发生,丹参酮可能通过抑制MIF保护淹溺性肺损伤.

Objective To observe the pathogenesis of seawater aspiration - induced lung injury, we determined T Ⅱ A attenuated the lung injury induced by seawater aspiration via negative regulation of MIF. Methods 24 rats were divided into normal group, seawater group, T Ⅱ A - treated group. In the seawater group rats were subjected to seawater aspiration. In the T Ⅱ A - treated group, rats received T Ⅱ A（25 mg/kg）intraperitoneally at 30 min after seawater aspiration. Results Seawater aspiration led to lung injury such as neutrophil infiltration, puhnonary edema and increase in microvascular permeability. MIF expression and levels of MPO in the lung were also elevated following seawater aspiration. However, these changes were attenuated by T I] A treatment. Conclusion our results suggested that T II A exerted a protection effects on the lung injury following seawater aspiration probably through inhibiting pro - inflammatory effect of MIF.