Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
Articles by R Hu
Total Records ( 1 ) for R Hu
  J Li , A Dai , R Hu , L Zhu and S. Tan

Oxidative stress is one of the major pathogenesis of chronic obstructive pulmonary disease (COPD). -Glutamylcysteine synthetase (-GCS) is one of the paramount antioxidant enzymes in COPD. Peroxisome proliferator-activated receptor-gamma (PPAR) is a ligand-activated transcription factor, which is activated by specific ligands such as rosiglitazone (RGZ), exerting multiple biological effects. PPAR coactivator-1 (PGC-1) is a PPAR coactivator, which binds to PPAR by induction of PPAR ligands, co-activating PPAR target genes. Growing evidence has suggested that PPAR/PGC-1 can regulate multiple antioxidant genes. However, the effect of PPAR/PGC-1 on -GCS during the development of COPD remains unclear. Here, we measured the expression levels of PPAR, PGC-1 and -GCS, -GCS activity and reactive oxygen species (ROS) contents in lungs of rats treated by cigarette smoke (CS) + lipopolysaccharide (LPS) and CS + LPS + RGZ, as well as lungs of patients suffered from COPD. Compared with lungs from CS + LPS-treated rats, lungs of RGZ-treated rats demonstrated markedly lower ROS contents, and remarkable increase of -GCS activity and increase of the expression levels of PPAR, PGC-1, and -GCS. Furthermore, compared with controls, expression levels of PPAR, PGC-1, and -GCS significantly increased in the lungs of mild COPD patients, and progressively decreased in lungs of patients with moderate and severe COPD. -GCS protein was positively correlated with FEV1%. PPAR and PGC-1 proteins were positively correlated with -GCS activity and mRNA level. In conclusion, -GCS showed compensatory upregulation in the early stage of COPD, which progressively decompensate with increasing COPD severity. The activation of the PPAR/PGC-1 pathway may protect against COPD progression by upregulating -GCS and relieving oxidative stress.

Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility