Shi Qiao, Liao Kang-Shu, Zhao Kai-Liang, Wang Wei-Xing, Zuo Teng, Deng Wen-Hong, Chen Chen, Yu Jia, Guo Wen-Yi, He Xiao-Bo, Abliz Ablikim, Wang Peng, Zhao Liang
Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Department of Hepatobiliary Surgery, Central Hospital of Enshi Autonomous Prefecture, Enshi, Hubei 445000, China.
Mediators Inflamm. 2015;2015:685043. doi: 10.1155/2015/685043. Epub 2015 Mar 23.
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.
氢气（H2）作为一种新型抗氧化剂，据报道可选择性地减少羟自由基（•OH）和过氧亚硝酸盐（ONOO-），并抑制某些促炎介质的产生，而不会干扰代谢氧化还原反应或细胞信号传导中涉及的活性氧（ROS）。我们在此旨在探讨其对牛磺胆酸钠诱导的急性胰腺炎中急性肾损伤的保护作用及其可能机制。大鼠成功建模后，通过尾静脉注射富氢盐水（HRS组）或生理盐水（SO和SAP组）（6 mL/kg），并皮下补充（20 mL/kg）。结果显示，富氢盐水减轻了以下各项：（1）血清肌酐和尿素氮；（2）胰腺和肾脏的病理损伤；（3）肾脏丙二醛（MDA）；（4）肾脏髓过氧化物酶（MPO）；（5）血清白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）以及肾脏肿瘤坏死因子-α（TNF-α）、高迁移率族蛋白B1（HMGB1）；（6）肾脏组织中的酪氨酸硝化、IκB降解和核因子κB（NF-κB）激活。此外，它还提高了肾脏组织中白细胞介素-10的水平和超氧化物歧化酶（SOD）的活性。这些结果证明，富氢盐水可减轻牛磺胆酸钠诱导的急性胰腺炎中的急性肾损伤，可能是由于其对过量ROS的解毒活性，并通过影响IκB硝化和降解来抑制NF-κB的激活。我们的研究结果突出了富氢盐水作为临床上治疗重症急性胰腺炎急性肾损伤新方法的潜在价值。
