Objective To investigate the effect of metformin (Met) on airway inflammation in rats with chronic obstructive pulmonary disease ( COPD) by regulating microRNA ( miR) - 34a. Methods The COPD rat model was established by fumigation for 30 min daily for 30 d and instillation of 2 mL lipopolysaccharide (LPS) solution through the airway on days 1, 14 and 28. Quantitative Real-time PCR ( qRT-PCR) was performed to detect the effect of Met on the miR-34a level in lung tissue; white blood cell count in bronchoalveolar lavage fluid (BALF) and wright staining were used to detect the effect of Met; hematoxylin-eosin (HE) was used to detect the effect of Met on lung morphology; the serum interleukin IL-6, IL-8, IL-1β and tumor necrosis factor-α (TNF-α) levels were detected by enzyme-linked immunosorbent assay; Western blot was used to detect the effect of Met on the sirt1 protein level in lung tissue; TargetScan was applied to determine the 3′UTR and miR-34a binding sites of sirt1 mRNA, and was identified by the dual luciferase reporter gene detection kit. Results Compared with the control group, in the model group the sirt1 protein level and the proportion of monocytes to macrophages in lung tissue were decreased ( P< 0. 05) , whereas the miR-34a level, the number of white blood cells in BALF, the proportions of neutrophils, eosinophils and lymphocytes, and the serum IL-6, IL-8, IL-1β and TNF-α levels were increased ( P< 0. 05) . Met in the COPD animals alleviated the reduced sirt1 protein level in lung tissues, the reduced proportion of monocytes to macrophages, and the increased miR-34a levels, number of white blood cells in BALF, proportions of neutrophils, eosinophils and lymphocytes, and the serum IL-6, IL-8, IL-1β and TNF-α levels (P<0. 05) . An increase of the miR-34a level reversed the effect of Met on COPD rats. Dual luciferase verified that miR-34a and sirt1 had a targeting relationship. Conclusions Met down-regulated miR-34a and thereby up-regulated sirt1 to relieve airway inflammation in COPD, which provides an experimental basis for the potential clinical treatment of COPD with Met.