Metformin attenuates fructose-induced pulmonary fibrosis, possibly through the involvement of the TRPC6 channel.

Pulmonary fibrosis is a chronic, progressive, fatal lung disease characterized by abnormal lung tissue repair and intense collagen accumulation in the lungs. Despite intensive efforts, no specific treatment has been found. The aim of this study was to investigate the effects of a high-fructose diet on lung tissue, whether the use of metformin corrects the damage caused by high fructose, and the possible relationship with transient receptor potential (TRP) channels. Lung damage was induced by adding 200 g/L fructose to the drinking water of Sprague-Dawley rats (n=32) for 10 weeks. In the groups in which the effect of metformin was examined, metformin (dissolved in saline) was administered intraperitoneally at a dose of 100 mg/kg in the last two weeks of the study. Inflammation and TRP channel levels were measured by ELISA. Histopathological evaluation was also assessed by Masson's Trichrome staining. A high-fructose diet caused collagen deposition, inflammation, and intra-alveolar hemorrhage in lung tissue. Interleukin-6 and TRPC6 channel protein levels in lung tissue were higher in the high-fructose group than in the control group. These effects were prevented by metformin treatment. Metformin administration and manipulation of TRPC6 channels may be a therapeutic target for the treatment of pulmonary fibrosis.