Selenium pretreatment improve renal function, autophagy signaling pathway and mir21a gene expression in renal ischemia reperfusion injury model in male rat.

Background: Renal ischemia-reperfusion injury (RIRI) is a major cause of acute kidney injury (AKI). Autophagy is an important mechanisms involved in this damage. In this study, we investigated effect of selenium on autophagy in kidney following IRI.

Methods: In this study, 24 Wistar male rats (200 ± 20 gr) were divided into 4 groups: 1) Sham 2) Sham+ Sodium selenite (0.5 mg/kg) 3) Ischemia-reperfusion (I/R) 4) I/R + sodium selenite. RIRI induces by vascular microclamp for 45 min. At the end of study, blood was taken from the heart tissue and used to measure BUN and Creatinine with the kit, the left kidney tissue was frozen for measurement of LC3II, LC3I, Beclin1, Rab11a, P62, and Caspase3 by western blot technique and measurement of mir21a by RT-PCR method. In addition, right kidney tissue was placed in formalin for histological studies with Haematoxylin‎‎-eosin staining.

Result: According to the results, in the I/R group compared to the sham group, serum levels of creatinine and urea, amount of autophagy including expression levels of Lc3II/Lc3I, beclin1, Rab11a, Cleaved Caspase3/Pro Caspase3 proteins significantly increased and expression of p62 decreased. Also, mir21a gene expression significantly decreased in the I/R group. According to histological results, ischemia-reperfusion has caused kidney tissue damage, such as destruction of the brush border of renal tubules, congestion, and leukocyte filtration. Our results showed that pretreatment with selenium reduced tissue damage and moderated the expression changes of the mentioned proteins.

Conclusion: It seems selenium inhibits autophagy by changing the expression levels of mediator molecules Rab11a and mir21a, and it can apply its healing effects in the damage caused by ischemia and reperfusion of kidney tissue in an animal model.