Histopathological changes and endoplasmic reticulum stress in type 1 diabetic mouse lung tissue

The aim of this study was to investigate the impact of type 1 diabetes on lung tissue using histopathological and immunohistochemical techniques, with a particular focus on whether it induces endoplasmic reticulum stress in the lung. The experiment utilized 18 male Balb/c mice, two months old with an average weight of 40 grams, randomly assigned to three groups: Control (n = 6), Sham (n = 6), and Streptozotocin diabetes group (n= 6). Diabetes was induced in the Streptozotocin group via a single intraperitoneal injection of 100 mg·kg-1 Streptozotocin. Following the experimental period, histopathological, immunohistochemical, and semi-quantitative analyses were conducted. Histopathological analysis revealed significant degeneration, apoptotic changes in epithelial cells and connective tissue, capillary dilation and inflammatory cell infiltration in the Streptozotocin group compared with the control and sham groups. Immunohistochemical analyses revealed a strong positive immunoreactivity for glucose regulated protein 78, nuclear factor kappa B and caspase–3 in type I and II pneumocytes, club cells, endothelial cells and alveolar macrophages in the Streptozotocin group. These observations imply the possible induction of endoplasmic reticulum stress in the lungs by type 1 diabetes and finally culminate into various histopathological alterations.