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 | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 14، دوره 26، شماره 1، فروردین 2023، صفحه 107-113 اصل مقاله (627.37 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2022.67042.14700 | ||
| نویسندگان | ||
| Rui-Jie Li1، 2؛ Chao-yan Wu1؛ Hao-liang Ke1؛ Xiu-ping Wang1؛ Ying-wen Zhang* 1، 2 | ||
| 1Department of Integrated Chinese and Western Medicine, Zhongnan Hospital of Wuhan University, Wuhan 430071, Hubei, China | ||
| 2School of Traditional Chinese Medicine, Hubei University of Chinese Medicine, Wuhan 430065, Hubei, China | ||
| چکیده | ||
| 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. | ||
| کلیدواژهها | ||
| Extracellular matrix؛ Lung diseases؛ NADPH oxidases؛ Oxidative stress؛ Pulmonary fibrosis؛ Renin-angiotensin system | ||
| مراجع | ||
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