氢生理盐水对大鼠肝脏缺血再灌注损伤的保护作用

Protective effect of hydrogen-rich saline on ischemia-reperfusion-induced liver injury in rats

目的探讨氢生理盐水（HS）对缺血再灌注肝损伤（I／R）的保护作用及机制。方法雄性SD大鼠60只随机分为3组：假手术组、对照组（I／R＋NS）、氢生理盐水治疗组（I／R＋HS）。缺血再灌注180min后检测血清肝功能，以及肝组织中丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽（GSH）、高迁移率族蛋白1（HMGB1）、肿瘤坏死因子a（TNF—a）、白介素1β（IL-1β）、白介素6（IL-6）含量，并用光镜观察肝细胞损伤和中性粒细胞浸润情况。结果缺血再灌注后，对照组大鼠肝功能水平明显降低，肝组织中MDA、HMGB1、TNF-a、IL-1β、IL-6含量明显升高，SOD和GSH水平显著降低，光镜下可见肝细胞大量变性坏死伴炎性细胞浸润。HS治疗组大鼠肝功能损伤明显减轻，氧化和炎性指标较对照组明显改善（P〈0．01）。结论HS能明显抑制大鼠缺血再灌注肝损伤，可能机制在于有效减轻氧化损伤及炎性反应。

Objective To study the effects of hydrogen-rich saline （HS） on the protection of hepatic injury induced by ischemia-reperfusion （I/R） in rats. Methods Male Sprague-Dawley rats （ n = 60） were randomly divided into three experimental groups： sham-operated group, I/R plus saline treatment group, and I/R plus hydrogen-rich saline treatment group. Reperfusion liver was conducted 180 mins after liver ischemia. Blood samples and liver tissues were collected. Result Serum ALT, AST levels, and MDA content, HMGB1, TNF-a, IL-1β and IL-6 levels in liver tissue were increased, but SOD and GSH activity were decreased significantly by I/R. Hydrogen-rich saline reduced oxidative stress and inflammatory reaction, and relieved morphological liver injury （P 〈 0. 01 ）. Conclusion Hydrogen-rich saline attenuated I/R induced liver damage by reduction of oxidative injury and inflammatory reaction.