XXVIII. World Congress World Association of Societies of Pathology and Laboratory Medicine (WASPALM): on the forefront of personalized medicine, Cancun, Mexico, 18 - 21 December 2015, pp.91
BACKGROUNDS Glucagon-like peptide-1 (GLP-1) stimulates mainly insulin secretion and displays extrapancreatic effects, such as anti-inflammatory role in atherosclerosis and surfactant-releasing effect in lungs. GLP-1 analogs are used in the treatment of diabetic patients. However, it is unclear therapeutic effect of exendin-4, a GLP-1 receptor agonist, on diabetes-mediated pulmonary complications. OBJECTIVE In this study, we aimed to investigate the effects of exendin-4 on lung injury seen in diabetic mice. METHOD BALB/c male mice were divided into four groups, in this study. The first group was given citrate buffer only, the second group was administered exendin-4 alone, the third group received streptozotocin (STZ), and the fourth group was given both STZ and exendin-4. Exendin-4 (3 g/kg) was administered by subcutaneous injection daily for 30 days after mice were rendered diabetic by administration of single dose STZ (200 mg/kg). RESULTS Lung structure, expressions of prosurfactant-C (proSPC), the receptor for advanced glycation end-products (RAGE), and production of reactive oxygen species (ROS) were evaluated in mice lungs. Diabetic mice lungs were characterized by an induced ROS production, edema, increase in the interstitial cell number, and the disruption of alveolar structure. Also, they possessed alveoli like honeycomb, thick alveolar walls and hypertrophic pneumocytes. Exendin-4 treatments resulted in the regression of edema and ROS production, the increased protein levels of proSPC and RAGE, and healing of alveolar structure. However, increase in cell number around bronchioles and venules was enormous in diabetic mice treated with exendin-4. A similar observation, but slightly, was obtained from control mice treated with exendin-4, as well. CONCLUSIONS Finally, exendin-4 might attenuate diabetes-mediated lung injury in mice, by inducing proliferation.