title: Investigation of the Hepato-Protective Effects of Imdur in a Rat Model of Chronic Mountain Sickness.
abstract: BACKGROUND
  The objective of this study was to determine if the clinical nitrate, Imdur, has a hepato-protective effect in chronic mountain sickness (CMS).
  
  
  METHODS
  A total of 60 SD rats were included in the study. Fifty rats were used to model CMS and were randomly divided into the following groups (10 rats per group): 1) plateau, 2) nifedipine, 3) low dose imdur, 4) moderate dose imdur, and 5) high dose imdur. The remaining 10 rats were used for the control group. Thirty days after the CMS model was established, according to the appropriate body weight of the rats, intragastric administration of the treatment groups commenced. After 15 days, changes in pulmonary artery pressure (PAP) and pathology of liver tissues were observed. Homocysteine (Hcy), interleukin-6 (IL-6), C-reactive protein (CRP), superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-PX) levels were also measured.
  
  
  RESULTS
  Compared with the control group, the levels of PAP, Hcy, IL-6, CRP, and MDA of the rats in the plateau model group, nifedipine group, and imdur groups were elevated. The levels of SOD and GSH-PX in these groups decreased relative to the control group. The injured rat livers were observed under the light microscope, revealing that hypoxia had caused tissue damage. Compared with that of the plateau model group, the levels of PAP, Hcy, IL-6, CRP, and MDA of the rats in the high dose imdur group were decreased (p < 0.05), and the levels of SOD and GSH-PX were increased (p < 0.05). Except for IL-6, the other parameters were comparable to normal values and better than those of the nifedipine group. Liver tissue from the high dose imdur group demonstrated less tissue damage from pathological sections.
  
  
  CONCLUSIONS
  High dose imdur has hepato-protective effects in CMS rat models.
authors.lastname: Wanglei
authors.forename: Dilinuer
authors.initials: D
authors.lastname: Maimaitiyimin
authors.forename: Yang
authors.initials: Y
authors.lastname: Tao
authors.forename: Wenhui
authors.initials: W
authors.lastname: Shi
authors.forename: Halmurat
authors.initials: H
authors.lastname: Upur
authors.forename: Ainiwaer
authors.initials: A
authors.lastname: Aikemu
mesh_terms: D000532:Altitude Sickness / Q000188:drug therapy* / Q000503:physiopathology; D000818:Animals; D015415:Biomarkers; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002097:C-Reactive Protein / Q000032:analysis; D002908:Chronic Disease; D005979:Glutathione Peroxidase / Q000097:blood; D006710:Homocysteine / Q000097:blood; D000860:Hypoxia / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D015850:Interleukin-6 / Q000097:blood; D007548:Isosorbide Dinitrate / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D008099:Liver / Q000187:drug effects* / Q000473:pathology; D008315:Malondialdehyde / Q000097:blood; D009543:Nifedipine / Q000494:pharmacology / Q000627:therapeutic use; D011651:Pulmonary Artery; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000097:blood; D013482:Superoxide Dismutase / Q000097:blood
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D017382:Reactive Oxygen Species; D006710:Homocysteine; D008315:Malondialdehyde; D002097:C-Reactive Protein; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D009543:Nifedipine; D007548:Isosorbide Dinitrate; C030397:isosorbide-5-mononitrate