Selenium Pretreatment Protects Against Renal Ischemia Reperfusion Injury by Inducing Mitochondrial Biogenesis

Background & Objective: Acute kidney injury (AKI) is a rapid loss of kidney function that is associated with high morbidity and mortality. Oxidative hazard, inflammation, mitochondrial deterioration and depletion of cellular energy stores, which terminate in organ dysfunction, are the major hallmarks of AKI. The current experimental investigation attempted to evaluate the effects of selenium (Se), a pivotal micronutrient, on the ischemia/reperfusion (IR)-induced kidney damage emphasizing on the biogenesis of mitochondria. Materials & Methods: Male Wistar rats (n = ۱۸) were randomly allocated into three groups: sham, IR, and Se + IR. Rats in the last group ۱ h before IR induction, were treated with Se (۰.۵ mg/kg) intraperitoneally. Six hours after reperfusion blood and kidney tissue samples were collected, and animals were euthanized. In addition to the evaluation of biochemical factors and histopathology, the protein levels of sirtuin۱ (SIRT-۱), and peroxisome proliferator-activated receptor-gamma coactivator ۱-α (PGC-۱α) of the kidney tissues were determined via western blotting. Results: Pre-treatment with Se could significantly improve IR-induced kidney function markers (creatinine and BUN) as well as the pathological alteration in comparison with the IR group (P < ۰.۰۵). Moreover, in the Se + IR group, a substantial surge of the Sirt-۱ and PGC-۱α at the protein level was recorded compared to the IR group. Conclusion: The results proposed that Se displays a protective role against renal IR injury via up-regulating proteins involved in mitochondrial biogenesis. Due to the pivotal role of mitochondria in renal tubules, these results offer insight into the plausible preventative and/or therapeutic effects of Se against AKI after further studies.

Keywords:

Selenium , Ischemia , Reperfusion Injury , Mitochondria , Sirtuins