title: Hind limb perconditioning renoprotection by modulation of inflammatory cytokines after renal ischemia/reperfusion.
abstract: Purpose Renal ischemia/reperfusion (I/R) injury is a common clinical problem associated with significant mortality and morbidity. One newly described strategy to reduce this damage is remote perconditioning (RPEC), in which short-time ischemia of a limb during renal ischemia reduces the I/R-induced kidney injury. This study aimed to assess whether RPEC confer protection through changes in pro-inflammatory mediators. Methods Rats were subjected to right nephrectomy and randomized into: sham (no intervention), I/R (subjected to 45-min left renal ischemia) and RPEC group (subjected to four cycles of 5-min I/R of the femoral artery administered during renal ischemia). After 24-h, blood, urine, and kidney samples were collected. Biochemical indicators of renal dysfunction were measured in the cases of Neutrophil gelatinase-associated lipocalin (NGAL), and N-acetyl-B-diglucosaminidase (NAG) activity. Inflammatory cytokines [interleukin (IL)-6 and tumor necrosis factor-alpha, TNF-α] expression in the renal tissues as well as Periodic acid-Schiff stained histological sections were evaluated. Results I/R resulted in renal dysfunction, as evidenced by higher renal NGAL expression and urinary NAG activities. This was accompanied by increased TNF-α and IL-6 expressions as well as histological changes in this group. However, RPEC improved renal histology and function compared with the I/R group. Furthermore, the RPEC group showed decreases in TNF-α and IL-6 expression. Conclusions These results suggest that RPEC reduces the dysfunction and injury associated with I/R of the kidney. This technique reduced the pro-inflammatory cytokine in the kidney. RPEC could be a promising strategy against I/R-induced acute kidney injury partly by down-regulation of inflammatory mediators.
authors.affiliation: a Department of Physiology, School of Medicine , Bushehr University of Medical Sciences , Bushehr , Iran ;|b Department of Physiology, School of Medicine , Tehran University of Medical Sciences , Tehran , Iran ;
authors.forename: Zahra
authors.initials: Z
authors.lastname: Sedaghat
authors.affiliation: b Department of Physiology, School of Medicine , Tehran University of Medical Sciences , Tehran , Iran ;
authors.forename: Mehri
authors.initials: M
authors.lastname: Kadkhodaee
authors.affiliation: b Department of Physiology, School of Medicine , Tehran University of Medical Sciences , Tehran , Iran ;
authors.forename: Behjat
authors.initials: B
authors.lastname: Seifi
authors.affiliation: c Department of Immunology, School of Medicine , Tehran University of Medical Sciences , Tehran , Iran.
authors.forename: Eisa
authors.initials: E
authors.lastname: Salehi
mesh_terms: D058186:Acute Kidney Injury / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D004195:Disease Models, Animal; D005121:Extremities / Q000098:blood supply; D007249:Inflammation / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood*; D019194:Ischemic Preconditioning / Q000379:methods*; D007668:Kidney / Q000098:blood supply*; D007677:Kidney Function Tests / Q000379:methods; D000071068:Lipocalin-2 / Q000097:blood*; D051381:Rats; D015427:Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015850:Interleukin-6; D000071068:Lipocalin-2; D014409:Tumor Necrosis Factor-alpha
keywords: Inflammation; ischemia; kidney; remote perconditioning; reperfusion injury