title: Rosiglitazone protects diabetic rats from liver destruction.
abstract: OBJECTIVE
  To investigate whether rosiglitazone (ROS) protects diabetic rats from destructive changes in the liver.
  
  
  METHODS
  Twenty-four Sprague Dawley rats were randomly divided into 3 groups: control (NC) group (no.=8), streptozocin (STZ)-treated diabetic (DM) group (no.=8), and STZ+ROStreated diabetic (RSG) group (no.=8). After 8 weeks, the liver structure was observed by light microscopy and transmission electron microscopy. Apoptosis was detected by TUNEL, and apoptosis index was calculated. The Fas ligand (FasL) mRNA expression of apoptosis-promoting gene and cyclooxygenase- 2 (COX-2) mRNA in the liver were detected by RTPCR. COX-2 protein in the liver was tested via immunohistochemical staining.
  
  
  RESULTS
  Compared to NC group, DM group showed a visible fatty degeneration and inflammatory cell infiltration in the liver under microscopy. Obvious hepatocyte swelling with atrophic mitochondria was observed, and the central zone of cholangiole was severely outstretched. Meanwhile, in RSG group, the hepatocyte steatosis and inflammatory cell infiltration decreased, and the hepatic ultra-structure was markedly improved. Hepatocyte apoptosis (p<0.05) and the expression levels for hepatic COX-2 mRNA (p<0.05), FasL mRNA (p<0.01), and COX-2 protein (p<0.05) were higher in DM group compared to the NC group, while the expression level of hepatic COX-2 mRNA (p<0.05), FasL mRNA (p<0.01), COX-2 protein (p<0.05), and hepatocyte apoptosis (p<0.05) in RSG group were decreased compared to DM group.
  
  
  CONCLUSIONS
  Diabetes causes severe liver injury and ROS can protect diabetic rats from liver destruction, which may be related to inhibition of the expression of COX-2 and the hepatocyte apoptosis induced by FasL gene over expression.
authors.affiliation: Division of Endocrinology and Metabolism, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China 200011. dryanginsh@yahoo.com
authors.forename: Y-L
authors.initials: YL
authors.lastname: Lu
authors.forename: T-T
authors.initials: TT
authors.lastname: Ye
authors.forename: Y
authors.initials: Y
authors.lastname: Chen
authors.forename: J
authors.initials: J
authors.lastname: Yu
authors.forename: L-J
authors.initials: LJ
authors.lastname: Zhao
authors.forename: N-J
authors.initials: NJ
authors.lastname: Wang
authors.forename: B-R
authors.initials: BR
authors.lastname: Jiang
authors.forename: J
authors.initials: J
authors.lastname: Qiao
authors.forename: L-Z
authors.initials: LZ
authors.lastname: Yang
mesh_terms: D000818:Animals; D017209:Apoptosis; D051546:Cyclooxygenase 2 / Q000096:biosynthesis / Q000235:genetics; D003921:Diabetes Mellitus, Experimental / Q000150:complications*; D053222:Fas Ligand Protein / Q000096:biosynthesis / Q000235:genetics; D005234:Fatty Liver / Q000209:etiology; D020287:In Situ Nick-End Labeling; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008107:Liver Diseases / Q000517:prevention & control*; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D000077154:Rosiglitazone; D045162:Thiazolidinediones / Q000627:therapeutic use*
chemical_list: D053222:Fas Ligand Protein; D012333:RNA, Messenger; D045162:Thiazolidinediones; D000077154:Rosiglitazone; D051546:Cyclooxygenase 2