Involvement of nuclear factor-kappa B on corticosterone-induced rat Leydig cell apoptosis

• Published in: Asian journal of andrology Vol. 8; no. 6; pp. 693 - 702
• Main Authors: Wang, Qian, Gao, Hui‐Bao
• Format: Journal Article
• Language: English
• Published: Melbourne, Australia Blackwell Publishing Asia 01.11.2006; Medknow Publications & Media Pvt. Ltd
• Subjects: Animals; apoptosis; Apoptosis - drug effects; Blotting, Western; corticosterone; Corticosterone - antagonists & inhibitors; Corticosterone - pharmacology; fas Receptor - immunology; Leydig Cells - drug effects; Male; Mifepristone - pharmacology; NF-kappa B - physiology; NF‐kappa B; rat Leydig cell; Rats; Rats, Sprague-Dawley; Transcription Factor RelA - biosynthesis; Transcription Factor RelA - physiology; 核因子抗体; 皮质脂酮; 细胞凋亡
• ISSN: 1008-682X; 1745-7262
• DOI: 10.1111/j.1745-7262.2006.00212.x

Aim： To investigate the activation of nuclear factor-kappa B （NF-kappa B） and its function in glucocorticoid-induced Leydig cell apoptosis. Methods： The 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 μmol/L Pyrrolidine dithiocarbamate （PDTC） on this apoptosis. Results： The 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. Conclusion： NF-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.