目的探讨地塞米松(DXM)对脓毒症急性肺肾损伤的影响及其可能机制。随机分配72只Wistar大鼠,建立对照组(NC)、脂多糖(LPS)和脂多糖地塞米松(LPS DXM)治疗组。 NC组大鼠注射生理盐水,LPS组注射LPS(5 mg/kg),LPS DXM组先注射LPS(5 mg/kg),后注射DXM(1 mg/kg)。采用ELISA法测定血清肿瘤坏死因子-α（TNF-α）和血清巨噬细胞炎症蛋白1α（MIP-1α）。在不同时间点测定肺湿/干重比、血清肌酐（SCR）和血尿素氮（BUN）。苏木精伊红染色（HE）用于观察肺和肾的病理变化。采用放射免疫法检测血浆、肺和肾组织中血管紧张素II（Ang II）的水平。采用免疫组化和蛋白质印迹（WB）检测肺和肾组织中血管紧张素II受体1型（AT1R）蛋白和血管紧张素II受体2型（AT2R）蛋白。采用硝酸还原酶法检测血清、肺、肾中一氧化氮(NO)水平。与对照组比较,血清TNF-α、MIP-1α、SCR、BUN、肺W/D、血浆Ang II水平, LPS组大鼠肺肾、肺肾AT2R蛋白、血清、肺肾中NO水平显着升高（P<0.05），肺肾组织出现病理损伤（P<0.05），而DXM则下调调节上述指标，减轻肺、肾组织的病理损伤。而肺和肾AT1R蛋白的表达与上述结果相反。脓毒症可引起急性肺和肾损伤，改变循环、肺和肾中RAAS成分。 DXM可改善脓毒症大鼠急性肺肾损伤，其机制可能与DXM下调炎症因子AngII、AT2R、NO和上调AT1R表达有关。版权所有：©2024 Zhan et al.这是一篇根据知识共享署名许可条款分发的开放获取文章，允许在任何媒体上不受限制地使用、分发和复制，前提是注明原始作者和来源。

To investigate the effect of dexamethasone (DXM) on acute lung and kidney injury with sepsis and its possible mechanism.Control (NC), lipopolysaccharide (LPS) and lipopolysaccharide + dexamethasone (LPS+DXM) treated groups were established by random assignment of 72 Wistar rats. The NC rats were injected with physiological saline, while the LPS group was injected with LPS (5 mg/kg) and LPS+DXM group was injected with LPS(5 mg/kg) first and followed by DXM (1 mg/kg). Serum tumor necrosis factor-α (TNF-α) and serum macrophage inflammatory protein 1α (MIP-1α) were measured by ELISA. Lung wet/dry weight ratio, serum creatinine(SCR) and blood urea nitrogen(BUN) were determined at various time points. Hematoxylin Eosin staining (HE) for pathological changes in the lung and kidney. Radioimmunoassay was used to detect the levels of angiotensin II (Ang II) in plasma, lung and kidney tissues. Immunohistochemistry and western blot (WB) were used to detect angiotensin II receptor type 1 (AT1R) protein and angiotensin II receptor type 2 (AT2R) protein in lung and kidney tissues. The level of nitric oxide (NO) in serum, lung and kidney were detected using nitrate reductase method.Compared with control group, serum TNF-α, MIP-1α, SCR, BUN, lung W/D, Ang II level in plasma, lung and kidney, lung and kidney AT2R protein, NO level in serum, lung and kidney were significantly elevated(P<0.05) and pathological damage of lung and kidney tissues were showed in LPS group rats (P<0.05), whereas DXM down-regulated the above indexes and alleviate pathological damage of lung and kidney tissues. However, the expression of the lung and kidney AT1R protein was opposite to the above results.Sepsis can cause acute lung and kidney injury and changes RAAS components in circulating, lung and renal. DXM can improve acute lung and kidney injury in septic rats, and the mechanism may be related to the down-regulation of inflammatory factors, AngII, AT2R, NO and up-regulation of AT1R expression by DXM.Copyright: © 2024 Zhan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.