Evaluation of VEGF, Cytokeratin-19 and Caspase 3 Immunolocalization in the Lung Tissue of Rat with Experimentally Induced Diabetes

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 the 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.

Deneysel Olarak Diyabet Oluşturulan Ratların Akciğer Dokusunun Caspase 3, Cytokeratin 19 ve VEGF İmmünolokalizasyonunun Değerlendirilmesi

Diabetes Mellitus (DM), akciğerlerin fonksiyonel yapısındaki değişikliklerle ve gaz değişimlerindeki bozukluklarla kendini gösterir. Diyabetik akciğer dokusunda bu değişiklikler çeşitli faktörlere bağlı olabilir. Bu çalışmada amacımız VEGF, CK19, kaspaz 3 immunolokalizasyonları ile ilgili olarak diyabetin akciğer dokusuna verdiği zararı ilişkilendirmektir. Çalışmada hayvanlar 4 gruba ayrıldı, deneysel diyabetli gruplara 60 mg/kg streptozotosin verildi ve kontrol grubuna serum fizyolojik solüsyonu intraperitoneal olarak verildi. Deneyin 7 ve 14. günlerinde diyabetik ve kontrol grupları sakrifiye edildi ve akciğer dokuları çıkarıldı. Doku örnekleri, standart ışık mikroskobu ile izlenerek histokimyasal ve immünhistokimyasal olarak değerlendirildi. Diyabetik grupta 7. ve 14. günlerde kontrol grubu ile kıyaslandığında CK19 ve Kaspaz 3 lokalizasyonu artmış, ancak VEGF immunolokalizasyonu azalmıştır. Bulgularımıza göre, akciğer dokusu diyabetin hedef organlarından biri olduğunu göstermektedir. Hiperglisemiye bağlı pulmoner parankimde artış fibrozis kaynağı olarak kabul edildi. Sonuç olarak, pulmoner fibrozis kaynağının CK19 immünolokalizasyonunun artmasına bağlı olarak, azalmış VEGF lokalizasyonunun, özellikle endotelyal hücrelerde, akciğer parankimindeki kan-hava bariyerinde önemli bir rolü olan, pulmoner kapiler endotelyumda apoptosisi arttırdığı sonucuna varıldı.

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