Evaluation of histopathological changes and exosomal biogenesis in pulmonary tissue of diabetic rats

Diabetes mellitus is one of the leading causes of death globally. The development of cellular injuries and impaired energy metabolism are involved in the pathogenesis of diabetes mellitus, leading to severe diabetic complications in different tissues such as the pulmonary tissue. Autophagy is a double-edged sword mechanism required for maintaining cell survival and homeostasis. Any abnormalities in autophagic response can lead to the progression of several diseases. Here, we aimed to assess the effect of diabetic conditions on the autophagic response and exosome secretion in a rat model of type 2 diabetes mellitus. The experimental diabetic group received 45.00 mg kg-1 streptozocin (STZ) dissolved in 0.10 M sodium citrate. After 4 weeks, we monitored autophagic response and exosome biogenesis in the pulmonary tract using immunohistochemistry (IHC) and Real-time polymerase chain reaction analyses, respectively. Histological examination revealed the interstitial bronchopneumonia indicating enhanced immune cell infiltration into the pulmonary parenchyma. Immunohistochemistry staining displayed an enhanced autophagic response through the induction of microtuble-associated protein light chain 3 (LC3) and protein sequestosome 1 (P62) compared to the control rats. These changes coincided with significant induction of tetraspanin CD63 in STZ-induced diabetic rats relative to control rats. In conclusion, a diabetic condition can increase the autophagic response in pulmonary tissue. The accumulation of P62 in the pulmonary niche exhibits an incomplete autophagic response. The abnormal autophagy response can increase pulmonary cell sensitivity against injuries.