Department of Respiratory Medicine, Tangdu Hospital, Fourth Military Medical University, Xi'an, PR China.
Pulm Pharmacol Ther. 2011 Dec;24(6):673-81. doi: 10.1016/j.pupt.2011.07.002. Epub 2011 Jul 27.
There is very little evidence on the value of administering estrogen in cases of seawater drowning which can induce acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Therefore, this study aimed to investigate whether 17β-estradiol (E2) treatment can attenuate seawater aspiration-induced ALI in rats. In the experiment, ALI was induced by endotracheal instillation of seawater (4mL/kg) and the rats were then given intraperitoneal injection of E2 (5mg/kg) 20min after seawater instillation. Finally, the changes of arterial blood gases which contained hydrogen ion concentration (pH), arterial oxygen tension (PaO(2)) and arterial carbon dioxide tension (PaCO(2)) were measured and the measurement of extravascular lung water (EVLW) was observed. The pulmonary histological changes were evaluated by hematoxylin-eosin stain. The expression of aquaporins (AQPs) 1, AQP5, and estrogen receptor-β (ERβ) was measured by western blotting and immunohistochemical methods. The results showed that compared with normal saline water, seawater aspiration induced more serious ALI in rats which was markedly alleviated by E2 treatment. Meanwhile, the ERβ in lung tissues was activated after E2 administration. The seawater aspiration group also presented with severe pulmonary edema which was paralleled with over expressed AQP1 and AQP5. However, the up-regulation of AQP1 and AQP5 was suppressed by the administration of E2, resulting in an attenuation of lung edema. In conclusion, E2 treatment could effectively attenuate seawater aspiration-induced acute lung injury in rats by the down-regulation of AQP1 and AQP5.
关于在海水溺水引起的急性肺损伤/急性呼吸窘迫综合征（ALI/ARDS）中给予雌激素的价值，几乎没有证据。因此，本研究旨在探讨 17β-雌二醇（E2）治疗是否可以减轻大鼠海水吸入性 ALI。在实验中，通过气管内滴注海水（4mL/kg）诱导 ALI，然后在海水滴注后 20 分钟给大鼠腹腔内注射 E2（5mg/kg）。最后，测量动脉血气中氢离子浓度（pH）、动脉氧分压（PaO2）和动脉二氧化碳分压（PaCO2）的变化，并观察血管外肺水（EVLW）的测量。通过苏木精-伊红染色评估肺组织学变化。通过 Western blot 和免疫组织化学方法测量水通道蛋白（AQPs）1、AQP5 和雌激素受体-β（ERβ）的表达。结果表明，与生理盐水相比，海水吸入在大鼠中引起更严重的 ALI，E2 治疗明显减轻了这种情况。同时，E2 给药后肺组织中的 ERβ被激活。海水吸入组还表现出严重的肺水肿，与过度表达的 AQP1 和 AQP5 平行。然而，E2 的给药抑制了 AQP1 和 AQP5 的上调，从而减轻了肺水肿。总之，E2 治疗可通过下调 AQP1 和 AQP5 有效减轻大鼠海水吸入性急性肺损伤。
