Effect of astragali injection on epithelial sodium channel expression in mice with acute lung injury.
- Author:
Yan ZHAO
1
;
Jing HE
;
Xian GUAN
;
Daoxin WANG
Author Information
- Publication Type:Journal Article
- MeSH: Acute Lung Injury; metabolism; Animals; Astragalus Plant; chemistry; Disease Models, Animal; Drugs, Chinese Herbal; pharmacology; Epithelial Sodium Channels; drug effects; metabolism; Interleukin-8; metabolism; Male; Mice; Mice, Inbred C57BL; Tumor Necrosis Factor-alpha; metabolism
- From: Journal of Southern Medical University 2012;32(11):1603-1605
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of astragali injection on the expression of epithelial sodium channel in mice with acute lung injury (ALI) and explore the possible mechanism.
METHODSThirty C57BL/6 mice were randomized into 3 equal groups, namely the control group, ALI model group, and astragali injection treatment group. Twelve hours after the treatments, The wet-dry ratio (W/D) of the lungs, inflammation cell percentages in the bronchoalveolar lavage fluid (BALF) and histopathological changes of the lung tissues were examined, and the expressions of α-ENaC, TNF-α, and IL-8 mRNA in the lung tissues were determined with quantitative RT-PCR.
RESULTSThe neutrophil percentage in the BALF increased significantly in ALI group as compared with that in the other two groups. Pathological examination revealed milder lung tissue inflammation, congestion and edema in astragalus injection treatment group than in the ALI model group. Compared with those in the control group, α-ENaC mRNA expression decreased significantly while TNF-α and IL-8 mRNAs increased markedly in ALI group. In astragalus injection treatment group, the expression level of α-ENaC mRNA was higher than that in ALI group, and TNF-α and IL-8 mRNA expression lower than those in ALI group but higher than those in the control group.
CONCLUSIONAstragalus injection can ameliorate ALI in mice by inhibiting the release of inflammatory factors and up-regulating ENaC mRNA expression to promote the clearance of pulmonary edema fluid.