Prolonged simvastatin treatment provided a decrease in apoptotic, inflammatory, and oxidative stress markers in ischemia-reperfusion-induced acute kidney injury model of rats
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Tarih
2021
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Sci Printers & Publ INC
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
OBJECTIVE: Ischemia-reperfusion (I/R) leads to reactive oxygen species formation and cell death in kidney tissue with injury and organ transplantation. Simvastatin (SIM) is an antioxidant, anti-inflammatory, and anticoagulant agent. Alterations in I/R-induced acute kidney injury model with SIM treatment were analyzed.
STUDY DESIGN: Wistar rats (n=28) were grouped into Sham, Ischemia, I/R, and I/R+ SIM treated. Left rat kidney renal vessels were clamped for 60 minutes for ischemia, and the I/R group had 6 hours of reperfusion. 10 mg/kg SIM was given orally for 28 days. MDA, GSH, and MPO were analyzed. Kidney tissues were paraffin embedded, and primary antibodies TNF-alpha and caspase-3 were applied for immunohistochemistry.
RESULTS: In the I/R group, intense inflammatory cell infiltration around the vessels and necrosis in the glomerular structures were observed. In the treated group, proximal and distal tubular cells were found to be close to normal. Immunoexpression of caspase-3 in the ischemia group was positive in degenerative glomeruli. In the treated group, TNF-alpha expression was negative in the glomerular structures. MDA and MPO levels were significantly increased in ischemia and I/R.
CONCLUSION: We suggest that SIM treatment improved kidney tissue structure and function in a model of I/R injury.
Açıklama
WOS:000708937900003
Anahtar Kelimeler
Caspase-3, Immunohistochemistry, Ischemia/reperfusion, Kidney, MPO, Simvastatin
Kaynak
Analytical and Quantitave Cytopathology and Histopathology
WoS Q Değeri
N/A
Scopus Q Değeri
Cilt
43
Sayı
4
Künye
Kafkaslı, A. ve Özkorkmaz, E.G. (2021). Prolonged simvastatin treatment provided a decrease in apoptotic, inflammatory, and oxidative stress markers in ischemia-reperfusion-induced acute kidney injury model of rats. Analytical and Quantitave Cytopathology and Histopathology, 43(4), 167-173.
