Naloxone Pretreatment Mitigates Secondary Renal Injury Following Hepatic Ischemia-Reperfusion in Rats
Keywords:
Saw Palmetto, Beta-Sitosterol, Pygeum Africanum, Phytotherapy, Benign Prostatic Hyperplasia, BPH 2.Abstract
Background: Hepatic ischemia–reperfusion (I/R) injury is a major complication of liver surgery and transplantation, often extending its harmful effects to distant organs such as the kidneys. Naloxone, a non-selective opioid receptor antagonist, has shown potential protective properties against I/R-induced tissue damage, but its role in renal protection following hepatic I/R remains unclear.
Objective: This study aimed to investigate the protective effects of naloxone pre-treatment on renal injury induced by hepatic I/R in rats.
Methods: The adult male albino rats (n=40) were subjected to a random division into four experimental cohorts: control, sham-operated, hepatic I/R, and naloxone + I/R.
Hepatic ischemia was induced by occluding the portal triad for 45 minutes, followed by 60 minutes of reperfusion. Serum ALT, AST, urea, and creatinine levels were measured, along with renal malondialdehyde (MDA) and TNF-α levels. Kidney tissues were evaluated histologically (H&E), immunohistochemically (COX-2, NF-κB, and caspase-3), and morphometrically.
Results: Hepatic I/R resulted in significant hepatic and renal dysfunction, oxidative stress, and inflammatory changes, evidenced by elevated serum biomarkers, disrupted renal histology, and increased COX-2, NF-κB, and caspase-3 expression. Naloxone pre-treatment markedly attenuated these alterations, preserving renal architecture, reducing oxidative stress, and lowering inflammatory and apoptotic marker expression.
Conclusion: Naloxone pre-treatment exhibits a protective effect against renal injury secondary to hepatic I/R by mitigating oxidative, inflammatory, and apoptotic pathways. These findings suggest its potential application as an adjuvant therapeutic strategy in liver surgery and transplantation.
