Bao Yuan decoction and Tao Hong Si Wu decoction improve lung structural remodeling in a rat model of myocardial infarction: Possible involvement of suppression of inflammation and fibrosis and regulation of the TGF-β1/Smad3 and NF-κB pathways

Chronic heart failure (CHF) leads to pulmonary structural remodeling, which may be a key factor for poor clinical outcomes in patients with end-stage heart failure, and few effective therapeutic options are presently available. The aim of the current study was to explore the mechanism of action and pulmonary-protective effects of treatment with Bao Yuan decoction combined with Tao Hong Si Wu decoction (BYTH) on lung structural remodeling in rats with ischemic heart failure. In a model of myocardial infarction (MI) induced by ligation of the left anterior descending (LAD) artery, rats were treated with BYTH. Heart function and morphometry were measured followed by echocardiography, histological staining, and immunohistochemical analysis of lung sections. The levels of transforming growth factor-beta l (TGF-beta 1), type I collagen, phosphorylated-Smad3 (p-Smad3), tumor necrosis factor-alpha (TNF-alpha), toll-like receptor 4 (TLR4), active nuclear factor kappa B (NF-kappa B) and alpha smooth muscle actin (alpha-SMA) were detected using Western blotting. Lung weight increased after an infarct with no evidence of pulmonary edema and returned to normal as a result of BYTH. In addition, BYTH treatment reduced levels of type I collagen, TGF-beta 1, and alpha-SMA expression and decreased the phosphorylation of Smad3 in the lungs of rats after ML BYTH treatment also reduced the elevated levels of lung inflammatory mediators such as TNF-alpha, TLR4, and NF-kappa B. Results suggested that BYTH could effectively improve lung structural remodeling after MI because of its anti-inflammatory and anti-fibrotic action, which may be mediated by suppression of the TGF-beta 1/Smad3 and NF-kappa B signaling pathways.