Impact of apoptosis and oxidative stress on pancreatic beta cell pathophysiology in streptozotocin-induced Type 1 diabetes mellitus

YAVUZ O., Dincel G. C., Yildirim S., El-Ashram S., Al-Olayan E.

TISSUE & CELL, cilt.91, 2024 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 91
  • Basım Tarihi: 2024
  • Doi Numarası: 10.1016/j.tice.2024.102552
  • Dergi Adı: TISSUE & CELL
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, Veterinary Science Database
  • Atatürk Üniversitesi Adresli: Evet

Özet

Aims: Hyperglycemia plays a crucial role in the islet cells, especially pancreatic beta cell death in type 1 diabetes mellitus (T1DM). However, a few research have concentrated on the pathophysiology of apoptosis and oxidative stress in T1DM. The aim of this study was to determine the expression of Caspase 3, Caspase 9, 8-OHdG, Glutathione Reductase, endothelial and inducible nitric oxide synthase in the pancreatic tissue of streptozotocin (STZ)-induced T1DM patients and to compare the cellular mechanisms underlying this metabolic disorder. Methods: For this purpose, a total of 20 Wistar albino rats were divided into two groups: Control (C) and Diabetes Mellitus (DM). In the DM group, T1DM was induced by STZ. Rats in the C group were injected intravenously with buffer solution. At the end of the day 20, rats were necropsied and immunohistochemical procedures were applied. Results: The immunohistochemical examination revealed, strong positive immunoreactions were observed in the islet cells of the DM groups, particularly when all antibody stains were considered. On the other hand, the C groups showed minimal changes. The difference between the C and DM groups in terms of all antibodies was statistically significant (p<0.01). Conclusions: In the present study, it was concluded that apoptosis, oxidative stress and NOS expressions were involved in islet cell destruction in pancreatic tissue in STZ-induced T1DM.