The optimal duration of ischemic preconditioning for renal ischemia-reperfusion injury in mice

Abstract

PurposeThe aim of the present study was to investigate the protective effects of ischemic preconditioning for different periods of time and to elucidate the optimal safe ischemic preconditioning time for renal ischemia-reperfusion (I/R) injury in mice.MethodsA total of 25 male C57BL/6 mice were randomly divided into 5 groups (sham, I/R, ischemic preconditioning [IP]-3, IP-5, and IP-7 groups), in which the kidney was preconditioned with IP of various durations and then subjected to I/R injury (the last 3 groups). To induce renal ischemia, the left renal pedicle was occluded with a nontraumatic microaneurysm clamp for 30 minutes followed by reperfusion for 24 hours. The effects of IP on renal I/R injury were evaluated in terms of renal function, tubular necrosis, apoptotic cell death and inflammatory cytokines.ResultsResults indicated that BUN and creatinine (Cr) levels increased significantly in the I/R group, but the elevations were significantly lower in IP groups, especially in the IP-5 group. Histological analysis revealed that kidney injury was markedly decreased in the IP-5 group compared with the I/R group, as evidenced by reduced renal necrosis/apoptosis. In addition, IP significantly inhibited gene expression of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and chemokines (monocyte chemoattractant protein-1). Western blot analysis indicated that the expression levels of Toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) were upregulated in the I/R group, while expression was inhibited in the IP groups.ConclusionFive-minute IP had the greatest protective effect against I/R injury.

Specific microRNAs are involved in the reno‑protective effects of sevoflurane preconditioning and ischemic preconditioning against ischemia reperfusion injury in rats

“…The sevoflurane APC effect on mice kidneys was also reported in vivo (13). As far as is known, although the efficacy of renal IPC has not yet been shown to be clinically significant, unlike remote IPC for the kidney, renal IPc in mice reportedly suppresses the cell-death caused by subsequent IRI (8,9).…”

“…Alleviation of IRI improves the prognosis of the preserved kidney (7). Previous animal studies reported that ischemic preconditioning (IPc) alleviates renal IRI (8,9) and numerous clinical studies have elucidated the IPc effects on the kidney. Furthermore, these surgeries are performed under general anesthesia.…”

Acute remote ischemic preconditioning alleviates free radical injury and inflammatory response in cerebral ischemia/reperfusion rats

“…During the inflammatory reaction, pro-inflammatory factors, including IL-6 and IL-1β, were released, and the level of anti-inflammatory cytokines (IL-10 and IL-1Ra) was decreased (53). Previous studies have indicated that IPreC markedly suppressed the gene expression level of pro-inflammatory factors (TNF-α, IL-1β, and IL-6) and chemokines in patients with renal IR injury (54). In addition, IPreC inhibited the release of IL-1β and enhanced the generation of IL-10 following IR in normal and steatotic livers (55).…”

Zinc Supplementation and Ischemia Pre-conditioning in Renal Ischemia/Reperfusion Injury

“…Renal ischemia/reperfusion (RIR) injury is a complex phenomenon, which disturbs renal function and induces kidney tissue damages (1, 2) resulting in acute kidney injury (AKI) (3). Clinically, RIR injury is occurred in different circumstances such as renal transplantation, renal surgeries, post-resuscitation shock, complex cardiovascular surgeries, and chemical agents/drugs induced renal toxicity (4, 5).…”

“…Clinically, RIR injury is occurred in different circumstances such as renal transplantation, renal surgeries, post-resuscitation shock, complex cardiovascular surgeries, and chemical agents/drugs induced renal toxicity (4, 5). Renal transplantation induced RIR injury increases renal dysfunction and mortality rate (3, 5). In general, ischemia followed by reperfusion induces reactive oxygen species (ROS) formation and inflammation, oxidative stress, mitochondrial damage, and apoptosis, which all contribute to renal disorder (3, 4).…”