title: Hydrogen-rich saline improves non‑alcoholic fatty liver disease by alleviating oxidative stress and activating hepatic PPARα and PPARγ.
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.
authors.affiliation: Graduate Management Unit, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Xiao
authors.initials: X
authors.lastname: Zhai
authors.affiliation: Department of Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Xiao
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Endocrinology, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Jiancan
authors.initials: J
authors.lastname: Lu
authors.affiliation: Department of Endocrinology, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Yaping
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Faculty of Naval Medicine, Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Xuejun
authors.initials: X
authors.lastname: Sun
authors.affiliation: Department of Endocrinology, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Qin
authors.initials: Q
authors.lastname: Huang
authors.affiliation: Department of Endocrinology, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China.
authors.forename: Qijin
authors.initials: Q
authors.lastname: Wang
mesh_terms: D000818:Animals; D015415:Biomarkers; D053148:Caspase 3 / Q000378:metabolism; D005951:Glucose Tolerance Test; D006859:Hydrogen; D007333:Insulin Resistance; D008297:Male; D065626:Non-alcoholic Fatty Liver Disease / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects* / Q000235:genetics; D047493:PPAR alpha / Q000235:genetics / Q000378:metabolism*; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D012965:Sodium Chloride / Q000737:chemistry* / Q000494:pharmacology*
chemical_list: D015415:Biomarkers; D047493:PPAR alpha; D047495:PPAR gamma; D012965:Sodium Chloride; D006859:Hydrogen; D053148:Caspase 3