Involvement of nuclear factor-kappa B on corticosterone- induced rat Leydig cell apoptosis.
- Author:
Qian WANG
1
;
Hui-Bao GAO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Blotting, Western; Corticosterone; antagonists & inhibitors; pharmacology; Leydig Cells; drug effects; Male; Mifepristone; pharmacology; NF-kappa B; physiology; Rats; Rats, Sprague-Dawley; Transcription Factor RelA; biosynthesis; physiology; fas Receptor; immunology
- From: Asian Journal of Andrology 2006;8(6):693-702
- CountryChina
- Language:English
-
Abstract:
AIMTo investigate the activation of nuclear factor-kappa B (NF-kappa B) and its function in glucocorticoid-induced Leydig cell apoptosis.
METHODSThe Leydig cells were isolated from male Sprague-Dawley rats (90 days of age) and were incubated with corticosterone (CORT, glucocorticoid in rat) for 6 h, 12 h and 24 h, respectively. The P65 subunit of NF-kappa B (NF-kappa B/P65) in nuclei and the inhibitor of NF-kappa B (Ikappa B) in cytoplasm were analyzed by Western-blotting. The Leydig cells were treated with anti-Fas antibody for 3 h followed by Western blotting to assay the changes of NF-kappa B/P65 in nuclei and in cytoplasm. The role of NF-kappa B in CORT-induced Leydig cell apoptosis was evaluated by observing the effects of NF-kappa B/P65 overexpression and inhibiting activation of NF-kappa B by 100 micromol/L Pyrrolidine dithiocarbamate (PDTC) on this apoptosis.
RESULTSThe treatment of Leydig cells with CORT increased the levels of NF-kappa B/P65 in nuclei and decreased the levels of Ikappa B in cytoplasm. Following the Leydig cells were treated with anti-Fas antibody, the levels of NF-kappaB/P65 was increased in nuclei and decreased in cytoplasm. The CORT-induced Leydig cell apoptosis was inhibited by overexpressed NF-kappaB/P65 and was enhanced by incubation with PDTC.
CONCLUSIONNF-kappa B is activated by increased FasL/Fas in CORT-induced Leydig cell apoptosis. NF-kappa B may play an anti-apoptotic role in this apoptosis.