氢生理盐水对GalN/LPS引起大鼠急性肝损伤的保护作用

Hydrogen-rich Saline Protects against Hepatotoxicity induced by GalN/LPS in Rats

目的研究氢生理盐水对GalN/LPS引起的大鼠急性肝损伤的保护作用并探讨其可能机制。方法将SD大鼠随机分为3组(n=20),除正常对照组外,均采用腹腔注射GalN/LPS造成急性肝损伤模型,并分别给予等量生理盐水或氢生理盐水(5 ml/kg,i.p.),24小时后检测血清肝功能,肝组织TNF-α、IL-1β水平及MDA、SOD、CAT、GSH活性,并用光镜观察肝细胞变性、死亡和炎细胞浸润情况。结果腹腔注射GalN/LPS后,GalN/LPS损伤组大鼠肝组织SOD、CAT、GSH水平及CYP2E1活性明显降低,血清ALT、AST及肝组织TNF-α、IL-1β、MDA含量明显升高,光镜下肝细胞大量变性坏死,并有中性粒细胞浸润。氢生理盐水治疗组大鼠肝功能显著好转,抗氧化能力明显增强,炎性指标显著低于对照组(P<0.01)。结论氢生理盐水能显著减轻GalN/LPS诱导大鼠急性肝损伤,并能有效增强抗氧化能力,抑制炎性反应。

Objective Hydrogen has been reported to selectively reduce the hydroxyl radical and alleviate acute oxidative stress in many models. Meanwhile, hydrogen-rich saline, which is easy and safe to apply, can avoid losing hydrogen into environment and provide higher and more accurate concentration of hydrogen. In this study, we investigated the effects of hydrogen-rich saline on the prevention of liver injury induced by GalN/LPS in rats. Male SD rats （ n = 60） were divided randomly into three experimental groups： sham operated, GalN/LPS plus saline treatment （5 ml/kg, i. p. ）, GalN/LPS plus hydrogen-rich saline treatment （5 ml/kg, i. p. ）. The liver damage was detected microscopically 24h after BDL. In addition, serum ALT, AST levels, and tissue TNF-α, IL- 1β, MDA content were all increased, hepatic SOD, CAT, GSH, and CYP2El-specific monooxygenase activity were all decreased significantly by GalN/LPS. Hydrogen-rich saline reduced these markers and relieved morphological liver injury （ P 〈 0. 1 ）. In conclusion, hydrogen-rich saline attenuates GalN/LPS induced liver damage possibly by reduction of oxidative stress and inflammatory reaction.