title: [Expression of COX-2 and PPARg in the livers of patients with acute on chronic HBV-related liver failure and their relationship with clinic parameters].
abstract: OBJECTIVE
  To study the expressions of cyclooxygenase-2 (COX-2) and Peroxisome proliferator-activated receptor gamma (PPARg) in liver of patients with hepatitis B virus (HBV) related acute-on-chronic liver failure (ACLF) and their correlation with clinical parameters.
  
  
  METHODS
  35 patients with ACLF, 35 patients with HBV related chronic liver failure (CLF), 27 patients with chronic hepatitis B(CHB) and 15 normal control were enrolled to study the expressions of COX-2 and PPARg in the liver tissues by immunohistochemical staining, and to analyze the correlation of the COX-2 and PPARg levels in liver tissues with clinical parameters.
  
  
  RESULTS
  COX-2 was distinctly expressed in the cytoplasm of the hepatocytes, but PPARg was mostly expressed in the nuclei of the hepatocytes and also could be seen in the cytoplasm. The expressions of COX-2 in the liver of ACLF, CLF and CHB groups increased significantly as compared with NC group (z = -5.18, -4.50, -5.32, P is less than 0.01). The levels of COX-2 in ACLF livers also increased evidently as compared with CLF groups (z = -1.98, P is less than 0.05). The expression levels of PPARg in ACLF liver tissues were much higher than the other three groups, and statistical significances existed between ACLF group and the other two groups (CLF, NC groups) (z = -2.62, -4.28, P is less than 0.01). In ACLF group, the expression of COX-2 correlated with MELD score (r = 0.337, P is less than 0.05) and the expression of PPARg correlated with HBV DNA load (r = 0.348, P is less than 0.05). Clinical data showed that the levels of AST, TBil, CHOL, PT, INR, FIB and MELD score in ACLF group were significantly different from that in CLF, CHB and NC groups.
  
  
  CONCLUSIONS
  COX-2 expressed in liver may be a marker to reflect the degree of inflammation and injury of liver tissue. The PPARg expression of liver could be increased during chronic HBV infection and may be a protective mechanism against liver injury.
authors.affiliation: Department of Infectious Diseases, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an 710061, China.
authors.forename: Ying-hua
authors.initials: YH
authors.lastname: Niu
authors.forename: Rui-tian
authors.initials: RT
authors.lastname: Yi
authors.forename: Hong-li
authors.initials: HL
authors.lastname: Liu
authors.forename: Tian-yan
authors.initials: TY
authors.lastname: Chen
authors.forename: Shu-lin
authors.initials: SL
authors.lastname: Zhang
authors.forename: Ying-ren
authors.initials: YR
authors.lastname: Zhao
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D051546:Cyclooxygenase 2 / Q000378:metabolism*; D058625:End Stage Liver Disease / Q000378:metabolism* / Q000821:virology; D005260:Female; D006515:Hepatitis B virus; D006801:Humans; D008099:Liver / Q000378:metabolism; D017114:Liver Failure, Acute / Q000378:metabolism* / Q000821:virology; D008297:Male; D008875:Middle Aged; D047495:PPAR gamma / Q000378:metabolism*; D055815:Young Adult
chemical_list: D047495:PPAR gamma; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human