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Mitochondria‐Targeted Antioxidant Peptide Promotes ATP Recovery and Reduces Renal Ischemia‐Reperfusion Injury
Author(s) -
Cheng FengYing,
Liu Shaoyi,
Darrah Shaun,
Zhao Zhihong,
Soong Yi,
Wu Dunli,
Szeto Hazel H
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.968.7
Subject(s) - oxidative stress , mitochondrion , mitochondrial permeability transition pore , inflammation , ischemia , pharmacology , reactive oxygen species , kidney , medicine , reperfusion injury , renal ischemia , renal function , antioxidant , chemistry , endocrinology , programmed cell death , apoptosis , biochemistry
SS‐31 is a mitochondria‐targeted small peptide that can inhibit mitochondrial permeability transition (MPT) and scavenge reactive oxygen species. The purpose of this study is to determine whether SS‐31, by protecting mitochondrial function and reducing oxidative damage during renal ischemia‐reperfusion (IR) injury, can reduce tubular cell death, inflammation, and promote epithelial regeneration. Male Sprague‐Dawley rats underwent bilateral renal ischemia for 45min. SS‐31 or saline was administered subcutaneously before ischemia as well as upon and after reperfusion. By treatment with SS‐31, animals show improved mitochondrial respiration and ATP production. Overall cell death, oxidative stress, and inflammation are reduced and renal function is improved. Furthermore, early signs of tubular regeneration are observed in SS‐31 treated group. SS‐31 represents a putative first‐in‐class therapeutic agent that can reduce renal IR injury and accelerate renal recovery. Our results support the hypothesis that MPT and oxidative stress underlie the inflammation and fibrosis induced by renal IR injury.