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

Qian Wang, Hui-Bao Gao

Department of Biochemistry and Molecular Biology, School of Medicine Shanghai Jiao Tong University, 280 South Chongqing Road, Shanghai 200025, China

DOI: 10.1111/j.1745-7262.2006.00212.x

Abstract
AIM: To investigate activation of NF-kappa B and its function in glucocorticoid-induced Leydig cell apoptosis. METHODS: The Leydig cells were isolated from male Sprague-Dawley rats (90 day of age). After Leydig cells were incubated with corticosterone (CORT, glucocorticoid in rat) for 6h, 12h and 24h, respectively, levels of NF-kappa B/P65 in nuclei and levels of Ikappa B in cytoplasm were analyzed by Western-blotting. The Leydig cells was treated with anti-Fas antibody for 6h and 12h followed by Western blotting to assay the changes in levels of NF-kappaB/P65 in nuclei and in cytoplasm. The role of NF-kappaB in CORT-induced Leydig cell apoptosis was evaluated by observing effects of NF-kappaB/P65 overexpression and inhibition of NF-kappa B activation by 100 μM Pyrrolidine dithiocarbamate (PDTC) on this apoptosis. RESULTS: The treatment of Leydig cells with CORT increased the levels of NF-kappaB/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-apoptosis role in this apoptosis.

Keywords: rat Leydig cell, NF-kappa B, apoptosis, corticosterone

Correspondence to: Prof. Hui-Bao Gao, Department of Biochemistry and Molecular Biology, School of Medicine Shanghai Jiao Tong University, 280 South Chongqing Road, Shanghai 200025, China
Tel: +86-21-6384-6590 ext.776453 Fax: 86-21-3406-0742
Email: gaohb@shsmu.edu.cn
Received 2006-02-11 Accepted 2006-06-05