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富氢盐水通过减轻氧化应激和激活肝脏中的过氧化物酶体增殖物激活受体α(PPARα)和过氧化物酶体增殖物激活受体γ(PPARγ)来改善非酒精性脂肪性肝病。

Hydrogen-rich saline improves non‑alcoholic fatty liver disease by alleviating oxidative stress and activating hepatic PPARα and PPARγ.

作者信息

Zhai Xiao, Chen Xiao, Lu Jiancan, Zhang Yaping, Sun Xuejun, Huang Qin, Wang Qijin

机构信息

Graduate Management Unit, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China.

Department of Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China.

出版信息

Mol Med Rep. 2017 Mar;15(3):1305-1312. doi: 10.3892/mmr.2017.6120. Epub 2017 Jan 13.

DOI:10.3892/mmr.2017.6120
PMID:28098910
Abstract

Non-alcoholic fatty liver disease (NAFLD) comprises a range of liver diseases, between steatosis and non‑alcoholic steatohepatitis and liver cirrhosis, which are closely associated with diabetes mellitus. Previous studies have indicated that oxidative stress is a key factor in the development of NAFLD. Molecular hydrogen (H2) may ameliorate oxidative stress injuries by selectively neutralizing peroxynitrite and hydroxyl radicals. The present study evaluated the effects of H2 on NAFLD in rats and concluded that H2‑rich saline had significant therapeutic effects on NAFLD induced by hyperglycemia and hyperlipidemia, as demonstrated by hematoxylin and eosin and terminal deoxynucleotidyl-transferase‑mediated dUTP nick end labeling staining. H2‑rich saline improved fasting blood glucose, fasting insulin, insulin sensitivity and glucose tolerance, and lowered the expression levels of tumor necrosis factor alpha, interleukin‑1 beta, 3‑nitrotyrosine and 8‑hydroxy‑2'‑deoxyguanosine in the liver. In addition, the present study revealed that H2‑rich saline could significantly increase peroxisome proliferator‑activated receptor (PPAR) α and PPARγ expression in hepatocytes. In conclusion, H2‑rich saline may significantly improve NAFLD, possibly by reducing oxidative stress and activating hepatic PPARα and PPARγ expression.

摘要

非酒精性脂肪性肝病(NAFLD)包括一系列肝脏疾病,从肝脂肪变性到非酒精性脂肪性肝炎以及肝硬化,这些疾病与糖尿病密切相关。先前的研究表明,氧化应激是NAFLD发生发展的关键因素。分子氢(H2)可通过选择性中和过氧亚硝酸盐和羟基自由基来减轻氧化应激损伤。本研究评估了H2对大鼠NAFLD的影响,结果表明,苏木精-伊红染色和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记染色显示,富氢盐水对高血糖和高脂血症诱导的NAFLD具有显著的治疗作用。富氢盐水改善了空腹血糖、空腹胰岛素、胰岛素敏感性和糖耐量,并降低了肝脏中肿瘤坏死因子α、白细胞介素-1β、3-硝基酪氨酸和8-羟基-2'-脱氧鸟苷的表达水平。此外,本研究还发现,富氢盐水可显著增加肝细胞中过氧化物酶体增殖物激活受体(PPAR)α和PPARγ的表达。总之,富氢盐水可能通过降低氧化应激和激活肝脏PPARα和PPARγ的表达来显著改善NAFLD。

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