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Hydrogen-rich saline attenuates acute renal injury in sodium taurocholate-induced severe acute pancreatitis by inhibiting ROS and NF-κB pathway.

Abstract
Hydrogen (H2), a new antioxidant, was reported to reduce (•)OH and ONOO(-) selectively and inhibit certain proinflammatory mediators to product, without disturbing metabolic redox reactions or ROS involved in cell signaling. We herein aim to explore its protective effects on acute renal injury in sodium taurocholate-induced acute pancreatitis and its possible mechanisms. Rats were injected with hydrogen-rich saline (HRS group) or normal saline (SO and SAP group) through tail intravenously (6 mL/kg) and compensated subcutaneously (20 mL/kg) after successful modeling. Results showed that hydrogen-rich saline attenuated the following: (1) serum Cr and BUN, (2) pancreatic and renal pathological injuries, (3) renal MDA, (4) renal MPO, (5) serum IL-1β, IL-6, and renal TNF-α, HMGB1, and (6) tyrosine nitration, IκB degradation, and NF-κB activation in renal tissues. In addition, it increased the level of IL-10 and SOD activity in renal tissues. These results proved that hydrogen-rich saline attenuates acute renal injury in sodium taurocholate-induced acute pancreatitis, presumably because of its detoxification activity against excessive ROS, and inhibits the activation of NF-κB by affecting IκB nitration and degradation. Our findings highlight the potential value of hydrogen-rich saline as a new therapeutic method on acute renal injury in severe acute pancreatitis clinically.
AuthorsQiao Shi, Kang-Shu Liao, Kai-Liang Zhao, Wei-Xing Wang, Teng Zuo, Wen-Hong Deng, Chen Chen, Jia Yu, Wen-Yi Guo, Xiao-Bo He, Ablikim Abliz, Peng Wang, Liang Zhao
JournalMediators of inflammation (Mediators Inflamm) Vol. 2015 Pg. 685043 ( 2015) ISSN: 1466-1861 [Electronic] United States
PMID25878401 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cytokines
  • NF-kappa B
  • Reactive Oxygen Species
  • 3-nitrotyrosine
  • Tyrosine
  • Sodium Chloride
  • Taurocholic Acid
  • Hydrogen
  • Amylases
Topics
  • Acute Disease
  • Acute Kidney Injury (drug therapy)
  • Amylases (blood)
  • Animals
  • Cytokines (biosynthesis)
  • Hydrogen
  • Kidney (pathology)
  • Male
  • NF-kappa B (antagonists & inhibitors, physiology)
  • Neutrophil Infiltration
  • Oxidative Stress
  • Pancreatitis (chemically induced, complications)
  • Rats
  • Rats, Wistar
  • Reactive Oxygen Species (metabolism)
  • Signal Transduction
  • Sodium Chloride (therapeutic use)
  • Taurocholic Acid (toxicity)
  • Tyrosine (analogs & derivatives, analysis)

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