Metformin, an oral first-line treatment for type 2 diabetes, reduces inflammation and pulmonary fibrosis in mice, a study published in the Journal of Korean Medical Science suggests. According to its authors, metformin (Glucophage) may be a therapy candidate for pulmonary fibrosis.
For the study, “Metformin Reduces Bleomycin-induced Pulmonary Fibrosis in Mice,” a team of researchers led by Dr. Young Whan Kim of the Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University College of Medicine, in South Korea, investigated the anti-fibrotic effects of metformin using a mouse model in which pulmonary fibrosis was induced with bleomycin.
The researchers took 62 mice and divided them into five groups. Mice in the first group were given bleomycin only (to induce fibrosis). Mice in the second and third group were given bleomycin and either a low dose (50 mg/kg) or a high dose (100 mg/kg) of metformin. Mice in the fourth group were given a high dose of metformin only (without inducing fibrosis), and those in the fifth group were used as a controls and did not receive any drug.
Scientists gave all the drugs orally once a day. On day 10, they sacrificed half of the mice in each group and analyzed their lungs. The remaining mice were sacrificed on day 21.
Researchers found that mice treated with bleomycin and metformin had significantly lower levels of inflammation in their lungs for both doses of metformin than animals given only bleomycin. The metformin-treated mice with induced pulmonary fibrosis also had less evidence of fibrosis than those mice given bleomycin but not treated with the diabetic drug. This was the case both on day 10 and day 21.
In addition, the researchers saw that on day 21, the levels of collagen, collagen-1, procollagen, fibronectin, and transforming growth factor-β, all indicative of the presence of fibrosis, were lower in mice treated with metformin compared to mice treated with bleomycin only.
They concluded that metformin could be a viable option for the treatment of pulmonary fibrosis. However, they recommend further research into understand the drug’s mechanism of action in pulmonary fibrosis before it might be considered for clinical use.
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