Protective Effects of Antioxidant Peptide SS-31 Against Multiple Organ Dysfunctions During Endotoxemia

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• 作者：Guoming Li ; Jing Wu ; Renqi Li ; Dong Yuan ; Yunxia Fan ; Jianjun Yang…
• 关键词：sepsis ; mitochondria ; inflammation ; oxidative stress ; apoptosis
• 刊名：Inflammation
• 出版年：2016
• 出版时间：February 2016
• 年：2016
• 卷：39
• 期：1
• 页码：54-64
• 全文大小：7,599 KB
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• 作者单位：Guoming Li (1)
  Jing Wu (2)
  Renqi Li (2)
  Dong Yuan (1)
  Yunxia Fan (1)
  Jianjun Yang (2)
  Muhuo Ji (2)
  Sihai Zhu (2)
  
  1. Department of Anesthesiology and Intensive Care, Jintan Hospital, Jiangsu University, Changzhou, China
  2. Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, 305 East Zhongshan, Road, Nanjing, 210002, China
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Rheumatology
  Internal Medicine
  Pharmacology and Toxicology
  Pathology
  
• 出版者：Springer Netherlands
• ISSN：1573-2576

文摘

Oxidative stress causes mitochondrial impairment, the failure of energy production, and consequent organ dysfunctions. The aim of the present study was to investigate the potential therapeutic effects of mitochondrial antioxidant SS-31 on sepsis-induced organ dysfunctions and to explore the possible mechanism. Sepsis was induced by cecal ligation and puncture. Immediately and at 5 h after the operation, SS-31 (5 mg/kg) or vehicle was administered intraperitoneally. The levels of organ dysfunctions, malondialdehyde, superoxide dismutase, proinflammatory cytokines, pulmonary wet-to-dry weight ratio, myeloperoxidase activity, histological scores, nuclear factor kappa B p65, inducible nitric oxide synthase, reactive oxygen species, adenosine triphosphate, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells were assessed at the indicated time points. The 7-day survival rate was estimated by the Kaplan-Meier method. In the present study, SS-31 treatment significantly improved sepsis-induced organ dysfunctions as evidenced by decreased histological scores, increased arterial partial oxygen tension, and deceased serum alanine aminotransferase, urea nitrogen, and creatinine levels, which was accompanied by decreased levels of malondialdehyde, tumor necrosis factor-alpha, pulmonary myeloperoxidase activity, nuclear factor kappa B p65, inducible nitric oxide synthase, reactive oxygen species, and TUNEL-positive cells. In conclusion, our data suggested that the protective effects of SS-31 on sepsis-induced organ dysfunctions were associated with the inhibition of proinflammatory cytokines, oxidative stress, and apoptosis. KEY WORDS sepsis mitochondria inflammation oxidative stress apoptosis