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Hum. Reprod. Advance Access originally published online on March 11, 2009
Human Reproduction 2009 24(7):1717-1725; doi:10.1093/humrep/dep058
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© The Author 2009. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Protective effect of curcumin in cisplatin-induced oxidative injury in rat testis: mitogen-activated protein kinase and nuclear factor-kappa B signaling pathways

Yusuf Ozlem Ilbey1,4, Emin Ozbek1, Mustafa Cekmen2, Abdulmuttalip Simsek1, Alper Otunctemur1 and Adnan Somay3

1 Department of Urology, Bezm-i Alem Valide Sultan Vakif Gureba Research and Education Hospital, Aksaray, Istanbul, Turkey 2 Department of Biochemistry, Kocaeli University, Kocaeli, Turkey 3 Department of Pathology, Bezm-i Alem Valide Sultan Vakif Gureba Research and Education Hospital, Istanbul, Turkey

4 Correspondence address. Tel: +90-212-534-69-70; Fax: +90-212-621-75-80; E-mail: ozlemyusufilbey{at}hotmail.com

BACKGROUND: The aim of this study was to investigate the cellular/biochemical mechanisms by which cisplatin (CIS) causes testicular toxicity. We evaluated the role of inducible nitric oxide synthase (iNOS) expression, mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kB) activation in the pathogenesis of testicular damage induced by CIS, and investigated the effects of curcumin (CMN) against CIS-induced testicular injury in rats.

METHODS: Rats were divided into five equal groups: (1) control, (2) CIS, (3) CMN, (4) CIS + CMN and (5) CIS + corn oil. After the treatment, body and testicular weights, and plasma testosterone levels were observed, along with the biochemical, histopathological and immunohistochemical changes in testes.

RESULTS: Testicular weight, plasma testosterone levels, activities of glutathione peroxidase (GSH-Px) and glutathione (GSH) levels significantly decreased, whereas the level of malondialdehyde (MDA) and nitric oxide (NO) significantly increased with CIS compared with the controls. A significant increase in plasma testosterone levels, GSH levels and GSH-Px activity, and a decrease in MDA and NO levels in testicular tissue were observed with CIS + CMN compared with that with CIS alone. There was marked staining for iNOS, MAPK/p38 and NF-kB/p65 expression with CIS compared with the control and CIS + CMN groups. CIS caused irregular seminiferous tubules, reduction of seminiferous epithelial layers, significant maturation arrest and perivascular fibrosis. CMN administration to CIS-treated rats significantly prevented these histopathologic changes.

CONCLUSIONS: MAPK and NF-kB activation have a significant role in CIS-induced testicular toxicity. CMN has a strong potential for use as a therapeutic adjuvant in CIS gonadotoxicity.

Key words: curcumin/nitric oxide/NF-kB/cisplatin/testicular damage

Submitted on July 24, 2008; resubmitted on February 10, 2009; accepted on February 12, 2009.


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