title: Effects of treatment with hydrogen sulfide on methionine-choline deficient diet-induced non-alcoholic steatohepatitis in rats.
abstract: OBJECTIVE
  Oxidative stress and inflammation play important roles in the progression from simple fatty liver to non-alcoholic steatohepatitis (NASH). The aim of this work was to investigate whether treatment with hydrogen sulfide (H2 S) prevented NASH in rats through abating oxidative stress and suppressing inflammation.
  
  
  METHODS
  A methionine-choline-deficient (MCD) diet rat model was prepared. Rats were divided into three experimental groups and fed for 8 weeks as follows: (i) control rats; (ii) MCD-diet-fed rats; (iii) MCD-diet-fed rats treated with NaHS (intraperitoneal injection of 0.1 mL/kg/day of 0.28 mol/L NaHS, a donor of H2 S).
  
  
  RESULTS
  MCD diet impaired hepatic H2 S biosynthesis in rats. Treatment with H2 S prevented MCD-diet-induced NASH, as evidenced by hematoxylin and eosin staining, reduced apoptosis and activities of alanine aminotransferase and aspartate aminotransferase, and attenuated hepatic fat accumulation in rats. Treatment with H2 S abated MCD-diet-induced oxidative stress through reducing cytochrome p4502E1 expression, enhancing heme oxygenase-1 expression, and suppressing mitochondrial reactive oxygen species formation, and suppressed MCD-diet-induced inflammation through suppressing activated nuclear factor κB signaling and reducing interleukin-6 and tumor necrosis factor α expressions. In addition, treatment of MCD-diet fed rats with H2 S had a beneficial modulation on expression profiles of fatty acid metabolism genes in livers.
  
  
  CONCLUSIONS
  Treatment with H2 S prevented NASH induced by MCD diet in rats possibly through abating oxidative stress and suppressing inflammation.
authors.affiliation: Department of General Surgery, General Hospital of Chengdu Military Command, Chengdu, Sichuan Province, China; Graduate School, The Third Military Medical University, Chongqing, China.
authors.forename: Zhu-Lin
authors.initials: ZL
authors.lastname: Luo
authors.forename: Li-Jun
authors.initials: LJ
authors.lastname: Tang
authors.forename: Tao
authors.initials: T
authors.lastname: Wang
authors.forename: Rui-Wu
authors.initials: RW
authors.lastname: Dai
authors.forename: Jian-Dong
authors.initials: JD
authors.lastname: Ren
authors.forename: Long
authors.initials: L
authors.lastname: Cheng
authors.forename: Ke
authors.initials: K
authors.lastname: Xiang
authors.forename: Fu-Zhou
authors.initials: FZ
authors.lastname: Tian
mesh_terms: D000818:Animals; D002796:Choline Deficiency / Q000150:complications*; D019392:Cytochrome P-450 CYP2E1 / Q000378:metabolism; D004195:Disease Models, Animal; D018450:Disease Progression; D005234:Fatty Liver / Q000150:complications / Q000209:etiology* / Q000517:prevention & control*; D051547:Heme Oxygenase-1 / Q000378:metabolism; D006862:Hydrogen Sulfide / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use*; D007249:Inflammation / Q000150:complications / Q000517:prevention & control; D015850:Interleukin-6 / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D008715:Methionine / Q000172:deficiency*; D008930:Mitochondria, Liver / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015850:Interleukin-6; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D008715:Methionine; D019392:Cytochrome P-450 CYP2E1; D051547:Heme Oxygenase-1; D006862:Hydrogen Sulfide
keywords: hydrogen sulfide; inflammation; methionine-choline deficient diet; non-alcoholic steatohepatitis; oxidative stress