Attenuation of NDEA-induced hepatocarcinogenesis by naringenin in rats
Article first published online: 21 NOV 2012
Copyright © 2012 John Wiley & Sons, Ltd.
Cell Biochemistry and Function
Volume 31, Issue 6, pages 511–517, August 2013
How to Cite
Subramanian, P. and Arul, D. (2013), Attenuation of NDEA-induced hepatocarcinogenesis by naringenin in rats. Cell Biochem. Funct., 31: 511–517. doi: 10.1002/cbf.2929
- Issue published online: 15 JUL 2013
- Article first published online: 21 NOV 2012
- Manuscript Accepted: 17 OCT 2012
- Manuscript Revised: 13 OCT 2012
- Manuscript Received: 12 SEP 2012
Chemoprevention is one of the most promising and realistic approaches in the prevention of cancer. Several bioactive compounds present in fruits and vegetables have revealed their cancer curative potential on hepatocellular carcinoma. Naringenin is one such naturally occurring flavonoid widely found in citrus fruits. In this study, we examined the molecular mechanisms by which naringenin inhibited NDEA-induced hepatocellular carcinoma in rats by analysing the expression patterns of proliferating cell nuclear antigen, Bcl-2, NF-κB, VEGF and MMP-2/9. Enhanced cell proliferation and apoptotic evasion in NDEA-induced hepatocarcinogenesis was associated with imbalance in pro-apoptotic and anti-apoptotic proteins together with upregulation of proliferating cell nuclear antigen (PCNA) and downregulation of caspase-3. Administration of pretreatment and posttreatment of naringenin decreased the expression of PCNA and Bcl-2 and increased the expression of Bax and caspase-3, indicating antiproliferative and apoptotic effects, respectively. Administration of NDEA increased the tumour expression of NF-κB, COX-2, VEGF, MMP-2 and MMP-9 that was correlated with more aggressive lesions and tumour growth. Downregulation of NF-κB, VEGF and MMPs by naringenin seen in the present study were correlated with the inhibition of liver tumour induced by NDEA. Our results suggest that naringenin could act as a legitimate agent by inhibiting cancer processes. Copyright © 2012 John Wiley & Sons, Ltd.