Dihydromyricetin Attenuates Bleomycin-induced Idiopathic Pulmonary Fibrosis and Improves Sport Endurance Performance of Mice

Background Interstitial pneumonia patients with idiopathic pulmonary fibrosis (IPF) have significantly reduced sport capacity. IPF can be treated with chemical drugs and hormones, but there are potential side effects such as digestive discomfort. Recently, natural products have been applied in the treatment of IPF. Dihydromyricetin (DHM) is a natural flavonoid extract of Garcinia cambogia , a grapevine plant, which has been shown to have significant anti-hepatic and renal fibrosis abilities, but its effects on IPF have not yet been studied. Objectives This study aimed to investigate the effects of DHM on IPF and sport capacity, as well as reveal the underlying mechanisms. Materials and Methods An IPF mouse model was induced with bleomycin, and then 50 mg/kg (DHM-L) and 100 mg/kg doses of DHM (DHM-H) were used to intervene in pulmonary fibrosis, and the effects of DHM on fibrotic lesions in lung tissue were observed using hematoxylin–eosin staining and Masson staining, and the effects of DHM on the sport ability were assessed by treadmill exercise. Results The fibrotic lesions in the lungs were obviously reduced in the DHM-L and DHM-H groups, and the levels of hydroxyproline, a marker of fibrosis, were significantly reduced; the inflammatory response was reduced, and the running time and distance of the mice on the treadmill were significantly increased. Western blot analysis showed that the key proteins in the interleukin-17 (IL-17) and transforming growth factor-β1 (TGF-β1)/smad signaling pathways were remarkably downregulated ( p < .05). The levels of fibrosis-associated proteins α-smooth muscle actin, vimentin, and collagen I were significantly decreased. Conclusion The present study showed that DHM attenuated bleomycin-induced IPF and improved sport endurance performance in mice, which was related to the inhibition of the IL-17 proinflammatory signaling pathway and the inhibition of the TGF-β1/smad profibrotic signaling pathway by DHM.