title: 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.
authors: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
authors: Qiao
authors: Q
authors: Shi
authors: Department of Hepatobiliary Surgery, Central Hospital of Enshi Autonomous Prefecture, Enshi, Hubei 445000, China.
authors: Kang-Shu
authors: KS
authors: Liao
authors: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
authors: Kai-Liang
authors: KL
authors: Zhao
authors: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
authors: Wei-Xing
authors: 0000-0002-3854-0083
authors: WX
authors: Wang
authors: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
authors: Teng
authors: T
authors: Zuo
authors: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
authors: Wen-Hong
authors: WH
authors: Deng
authors: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
authors: Chen
authors: C
authors: Chen
authors: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
authors: Jia
authors: J
authors: Yu
authors: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
authors: Wen-Yi
authors: WY
authors: Guo
authors: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
authors: Xiao-Bo
authors: XB
authors: He
authors: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
authors: Ablikim
authors: A
authors: Abliz
authors: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
authors: Peng
authors: P
authors: Wang
authors: Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
authors: Liang
authors: L
authors: Zhao
mesh_terms: D000208:Acute Disease; D058186:Acute Kidney Injury / Q000188:drug therapy*; D000681:Amylases / Q000097:blood; D000818:Animals; D016207:Cytokines / Q000096:biosynthesis; D006859:Hydrogen; D007668:Kidney / Q000473:pathology; D008297:Male; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000502:physiology; D020556:Neutrophil Infiltration; D018384:Oxidative Stress; D010195:Pancreatitis / Q000139:chemically induced / Q000150:complications*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction; D012965:Sodium Chloride / Q000627:therapeutic use*; D013656:Taurocholic Acid / Q000633:toxicity*; D014443:Tyrosine / Q000031:analogs & derivatives / Q000032:analysis
chemical_list: D016207:Cytokines; D016328:NF-kappa B; D017382:Reactive Oxygen Species; C002744:3-nitrotyrosine; D014443:Tyrosine; D012965:Sodium Chloride; D013656:Taurocholic Acid; D006859:Hydrogen; D000681:Amylases