Open AccessThe protective effects of tadalafil on renal damage following ischemia reperfusion injury in rats
Author(s) -
Erol Bulent,
Turker Tugrul,
Tok Adem,
Bektas Sibel,
Mungan Gorkem,
Ozkanli Seyma,
Karakas Bugra,
Tokgoz Husnu,
Akduman Bulent,
Mungan Aydin
Publication year - 2015
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1016/j.kjms.2015.06.005
Subject(s) - tadalafil , medicine , malondialdehyde , nitric oxide synthase , nitric oxide , pharmacology , ischemia , reperfusion injury , antioxidant , renal ischemia , endocrinology , oxidative stress , biochemistry , erectile dysfunction , chemistry
Ischemia‐reperfusion injury can cause renal damage, and phosphodiesterase inhibitors are reported to regulate antioxidant activity. We investigated the prevention of renal damage using tadalafil after renal ischemia reperfusion (I/R) injury in rats. A total of 21 adult male Wistar albino rats were randomly divided into three groups of seven, including Group 1‐control, Group 2‐I/R, and Group 3‐tadalafil + I/R group (I/R‐T group) received tadalafil intraperitoneally at 30 minutes before ischemia. Inducible nitric oxide synthase, endothelial nitric oxide synthase, malondialdehyde, and total antioxidant capacity levels were evaluated, and histopathological changes and apoptosis in the groups were examined. Tadalafil decreased malondialdehyde levels in the I/R group and increased the total antioxidant capacity level. Histopathological and immunohistochemical findings revealed that tadalafil decreased renal injury scores and the ratios of injured cells, as measured through apoptotic protease activating factor 1, inducible nitric oxide synthase, and endothelial nitric oxide synthase levels. We suggest that tadalafil has protective effects against I/R‐related renal tissue injury.