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高压氧疗法通过上调水通道蛋白1(AQP1)和水通道蛋白5(AQP5)的表达减轻脂多糖诱导的大鼠急性肺损伤。

Hyperbaric oxygen therapy palliates lipopolysaccharide-induced acute lung injury in rats by upregulating AQP1 and AQP5 expression.

作者信息

Han Guang, Ma Ling, Guo Yao, Li Lu, Li Dan, Liu Hongtao

机构信息

a Department of Anesthesia , Shengjing Hospital of China Medical University , Shenyang , Liaoning , China.

出版信息

Exp Lung Res. 2015;41(8):444-9. doi: 10.3109/01902148.2015.1064189. Epub 2015 Aug 28.

DOI:10.3109/01902148.2015.1064189
PMID:26317897
Abstract

PURPOSE

Hyperbaric oxygen (HBO) therapy has been suggested to palliate acute lung injury (ALI), but the mechanisms involved are not well understood. This study is to elucidate the involvement of AQP1 and AQP5 in the HBO related ALI therapy.

MATERIALS AND METHODS

lipopolysaccharide (LPS) was administrated into SD rats to obtain ALI models. Pressure of oxygen (PaO2) and carbon dioxide (PaCO2) in arterial blood and oxygenation index in rats after LPS and HBO treatments were determined. Pathological changes of the lungs were examined by hematoxylin and eosin staining. Alteration of TNF-α level during LPS and HBO treatments was evaluated with ELISA analysis. Western blot was employed to assess the expression of AQP1 and AQP5.

RESULTS

Blood gas indexes were largely decreased by LPS administration, which responded to HBO. Pathological examination showed that the inflammation symptoms in lungs induced by LPS were also palliated after HBO preconditioning. LPS induced the expression of TNF-α at a high level which could be downregulated by HBO and TNF-α antagonist treatments. Results of AQP1 and AQP5 determination found that HBO and TNF-α antagonist would upregulate the expression of AQP1 and AQP5 which was inhibited in rats with ALI.

CONCLUSIONS

HBO therapy palliated LPS-induced ALI in rats by downregulating TNF-α expression. HBO also upregulated AQP1 and AQP5 expression. These results could serve as guidelines for the full understanding of ALI therapy by HBO, thus achieving maximized therapeutic efficiency.

摘要

目的

高压氧(HBO)疗法已被建议用于缓解急性肺损伤(ALI),但其涉及的机制尚不清楚。本研究旨在阐明水通道蛋白1(AQP1)和水通道蛋白5(AQP5)在HBO相关ALI治疗中的作用。

材料与方法

将脂多糖(LPS)注入SD大鼠以建立ALI模型。测定LPS和HBO处理后大鼠动脉血中的氧分压(PaO2)、二氧化碳分压(PaCO2)及氧合指数。通过苏木精-伊红染色检查肺组织的病理变化。采用酶联免疫吸附测定(ELISA)分析评估LPS和HBO处理期间肿瘤坏死因子-α(TNF-α)水平的变化。采用蛋白质免疫印迹法评估AQP1和AQP5的表达。

结果

LPS给药后血气指标大幅下降,HBO治疗后有所改善。病理检查显示,HBO预处理后,LPS诱导的肺部炎症症状也得到缓解。LPS诱导TNF-α高水平表达,HBO和TNF-α拮抗剂处理可使其下调。AQP1和AQP5的测定结果发现,HBO和TNF-α拮抗剂可上调ALI大鼠中被抑制的AQP1和AQP5的表达。

结论

HBO疗法通过下调TNF-α表达缓解LPS诱导的大鼠ALI。HBO还上调了AQP1和AQP5的表达。这些结果可为全面理解HBO治疗ALI提供指导,从而实现最大治疗效果。

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