Title of article :
Qing Fei Hua Xian Decoction ameliorates bleomycin-induced pulmonary fibrosis by suppressing oxidative stress through balancing ACE-AngII-AT1R/ACE2-Ang-(1-7)-Mas axis
Author/Authors :
Li ، Rui-Jie Department of Integrated Chinese and Western Medicine - Zhongnan Hospital of Wuhan University , Wu ، Chao-yan Department of Integrated Chinese and Western Medicine - Zhongnan Hospital of Wuhan University , Ke ، Hao-liang Department of Integrated Chinese and Western Medicine - Zhongnan Hospital of Wuhan University , Wang ، Xiu-ping Department of Integrated Chinese and Western Medicine - Zhongnan Hospital of Wuhan University , Zhang ، Ying-wen Department of Integrated Chinese and Western Medicine - Zhongnan Hospital of Wuhan University
From page :
107
To page :
113
Abstract :
Objective(s): We aimed to investigate the preventative effect of Qing Fei Hua Xian Decoction (QFHXD) against pulmonary fibrosis (PF) and its potential mechanisms. Materials and Methods: Bleomycin (BLM)-induced rats were respectively treated with 413.3, 826.6, and 1239.9 mg/kg of QFHXD and prednisone for 28 days. The lung tissues of rats were collected on day 28 for histological and western blotting analysis. Results: QFHXD significantly reduced alveolus inflammation, collagen accumulation, and fibrosis deposition in BLM-induced PF rats (P 0.05). Collagen I and III, vimentin, and α-smooth muscle actin(α-SMA) expression levels were likewise decreased in PF rats treated with QFHXD (P 0.05). Additionally, QFHXD increased the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) while decreasing NADPH oxidase 4 (NOX4) expression (P 0.05). Furthermore, QFHXD suppressed the PF progression by down-regulating Angiotensin-Converting Enzyme (ACE) -Angiotensin II (AngII) -Angiotensin II Type 1 Receptor (AT1R) axis (P 0.01) and up-regulating Angiotensin-Converting Enzyme 2 (ACE2) -Angiotensin-(1-7) (Ang-(1-7)) -Mas axis (P 0.05). Conclusion: QFHXD suppressed inflammatory infiltration and PF brought on by BLM in lung tissues through reducing oxidative stress by maintaining the equilibrium of ACE-AngII-AT1R and ACE2-Ang-(1-7) -Mas axes. This study may provide a novel clinical therapy option for PF.
Keywords :
Extracellular matrix , Lung Diseases , NADPH oxidases , Oxidative stress , Pulmonary Fibrosis , Renin , angiotensin system
Journal title :
Iranian Journal of Basic Medical Sciences
Journal title :
Iranian Journal of Basic Medical Sciences
Record number :
2745588
Link To Document :
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