title: [Gene expression changes of regucalcin and prohibitin in cirrhotic rat liver and the related effects of compound glutathione inosine injection intervention].
abstract: OBJECTIVE
  To study expression of regucalcin (RGN) and prohibitin (PHB) genes in cirrhotic rat liver and to investigate the related effects of compound glutathione inosine injection (CGII) intervention.
  
  
  METHODS
  Forty male Wistar rats were randomly divided into a control group (n=12) and a model group (n=28).The model was established by injecting sterile porcine serum (0.5 mL) into the rat abdominal cavity, twice weekly for 8 consecutive weeks; the control group rats were treated with physiological saline injection (0.5 mL) into the abdominal cavity with the same frequency and time span. During the modeling period, four rats from the model group were randomly selected at different time points to examine changes in liver pathology. Upon pathology confirmation of liver cirrhosis, the porcine serum injection was terminated. The remaining 24 rats in the model group were randomly divided into a fibrosis group and a CGII treatment group.The CGII group received CGII (intramuscular injection of 0.018 mL 100g-1 body weight) once a day for 6 continuous weeks; the fibrosis rats were treated with the same dosage of physiological saline with the same frequency and time span.Liver tissue morphology was examined by both hematoxylin-eosin and Masson's staining. RGN and PHB expression at the mRNA and protein levels in liver tissues were detected by real time RT-PCR and immunohistochemical staining, respectively.
  
  
  RESULTS
  Both the mRNA and protein expression levels of RGN and PHB were significantly lower in the liver tissues of the fibrosis group than in the control group.CGII intervention led to significant alleviation of the liver fibrosis severity; moreover, the mRNA and protein expression levels of RGN and PHB were significantly higher than those in the fibrosis group.
  
  
  CONCLUSIONS
  Down-regulation of regucalcin and prohibitin gene expression might contribute to the pathogenesis of liver cirrhosis.
authors.affiliation: Zhoukou City Center Hospital Digestive Department Award, Henan 466000, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Liu
authors.forename: Jun
authors.initials: J
authors.lastname: Wu
authors.forename: Yue-Dong
authors.initials: YD
authors.lastname: Liang
authors.forename: Shuang
authors.initials: S
authors.lastname: Lu
authors.forename: Ming-Liang
authors.initials: ML
authors.lastname: Cheng
authors.forename: Jun-Ying
authors.initials: JY
authors.lastname: Liu
mesh_terms: D000818:Animals; D002135:Calcium-Binding Proteins / Q000235:genetics*; D002265:Carboxylic Ester Hydrolases; D015536:Down-Regulation; D015870:Gene Expression; D005978:Glutathione / Q000633:toxicity*; D007288:Inosine; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics*; D008103:Liver Cirrhosis / Q000235:genetics*; D008297:Male; D000091402:Prohibitins; D051381:Rats; D017208:Rats, Wistar; D012097:Repressor Proteins / Q000235:genetics*
chemical_list: D002135:Calcium-Binding Proteins; D047908:Intracellular Signaling Peptides and Proteins; C000717332:Phb protein, rat; D000091402:Prohibitins; D012097:Repressor Proteins; D007288:Inosine; D002265:Carboxylic Ester Hydrolases; C513325:Rgn protein, rat; D005978:Glutathione