Diabetes Mellitus (DM) manifests itself with changes in the functional structure of the lungs and impairments in gas exchange. These changes in diabetic lung tissue may be due to various factors. Our aim in this study is to correlate the damage of diabetes with lung tissue in terms of VEGF, CK19, caspase 3 immunolocalizations. In this study, animals were divided into 4 groups, 60 mg/kg streptozotocin was given to each of the groups with experimental diabetes and the physiological saline solution was given intraperitoneally to the control group. On days 7 and 14 of the experiment, diabetic and control groups were euthanized, and lung tissues were removed.Tissue samples were evaluated histochemically and immunohistochemically by monitoring with standard light microscopy. In the diabetic group, the localization of CK19 and Caspase 3 increased on the 7th and 14th days compared to t he control group, but the immunolocalization of VEGF decreased. Based on our findings, it was determined that lung tissue was one of the target organs of diabetes.The increase in pulmonary parenchyma due to hyperglycemia is accepted as a source of fibrosis. We concluded that due to increased CK19 localization of fibrosis source, decreased VEGF localization has increased apoptosis in the pulmonary capillary endothelium, which has a significant role in the blood-air barrier in the lung parenchyma, especially in endothelial cells.