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口服富氢水对小鼠脂肪肝缺血再灌注损伤的保护作用 被引量:4

Hydrogen-rich water alleviates ischemia-reperfusion injury in mice with fatty liver
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摘要 目的探讨富氢水对脂肪肝缺血再灌注损伤小鼠模型的保护作用。方法将30只C57BL/6小鼠随机分为3组。假手术组:喂蛋氨酸胆碱缺乏高脂饮食非酒精性脂肪肝造模;对照组:肝脏缺血再灌注前灌服蒸馏水;富氢水缺血再灌注组:肝脏缺血再灌注前灌服富氢水,再灌注6 h后处死小鼠,检测血清中AST和ALT含量,观察肝脏组织形态学变化,分析肝脏组织损伤程度、巨噬细胞浸润、炎性因子TNF-α、IL-6、OPN mRNA表达水平和肝脏组织内活化的Caspase-3蛋白表达水平。结果与对照组相比较,富氢水组血清ALT和AST水平较低(P<0.05),巨噬细胞浸润和凋亡细胞明显减少,炎性因子mRNA的表达明显降低。Caspase-3表达明显降低。结论富氢水能够减轻脂肪肝小鼠肝脏缺血再灌注损伤,其机制与富氢水抑制氧化应激反应和炎症反应,进而抑制Caspase-3蛋白表达有关。 Objective To explore the protective effect of hydrogen-rich water on liver ischemia-reperfusion (I/R)in mice models with fatty liver and the possible mechanism.Methods A total of 30 C57BL/6 mice were randomly divid-ed into 3 groups:sham-operated group (SO),control group (mice with steatotic liver perfused with water before ische-mia induction)and hydrogen-rich water group (mice with steatotic liver perfused with hydrogen-rich water before ische-mia reperfusion).Six hours after reperfusion,the mice were sacrificed,and serum and liver samples were collected. The ALT and AST levels in serum were determined and liver histological damage was evaluated.The infiltration of macrophages was detected.The mRNA expressions of TNF-α,IL-6,and OPN mRNA were assayed using real-time re-verse transcription PCR.The expression of activated Caspase-3 was checked with Western blotting.Results Compared with control group,6 hours following reperfusion,mice in hydrogen-rich water group exhibited lower levels of ALT and AST (P〈0.05),lower expression of inflammatory cytokines and Caspase-3,milder histological damage,and less in-filtration of macrophages (P〈0.05 ).Conclusion Hydrogen-rich water given by gavage can alleviate steatotic liver ischemia-reperfusion injury by inhibiting oxidant stress,inflammatory response and apoptosis induced by reperfusion.
出处 《山东大学学报(医学版)》 CAS 北大核心 2015年第1期10-15,共6页 Journal of Shandong University:Health Sciences
基金 内蒙古自然科学基金重大项目(2010ZD10)
关键词 富氢水 非酒精性脂肪肝 缺血再灌注损伤 氧化应激 炎症反应 Hydrogen rich water Nonalcoholic fatty liver Reperfusion injury Oxidant stress Inflammatory
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