<?xml version="1.0" encoding="utf-8"?>
<Journal>
<Journal-Info>
<name>International Journal of Pharma and Bio Sciences</name>
<website>ijpbs.net</website>
<email>editorijpbs@rediffmail.com (or) editorofijpbs@yahoo.com (or) prasmol@rediffmail.com</email>
</Journal-Info>
<article>
<article-id pub-id-type='other'>10.22376/ijpbs.2019.10.1.p1-12</article-id>
<issue_number>Volume 7 Issue 3</issue_number>
<issue_period>2016 (July - September)</issue_period>
<title>DOWNREGULATION OF TNF-α, NF-κB p65, COX-2 AND iNOS BY β-SITOSTEROL AMELIORATE THE TOXIC EFFECT OF Fe-NTA ON RENAL TISSUE</title>
<abstract>The success of dysregulated NF-κB activated genes inhibition by phytosterols has encouraged in targeted therapy of chronic inflammatory diseases. The objective of this current study was to examine the involvement of β-sitosterol in the inflammatory cascade against renal carcinogen. Renal cancer was induced by single intraperitoneal injection of N-diethylnitrosamine (200 mg/kg bw) and twice weekly administration of ferric nitrilotriacetate (9 mg Fe/kg bw) for 16 weeks. The chemopreventive potential of β- sitosterol against renal carcinogen was studied in terms of inflammatory markers. Our study showed that oral administration of β-sitosterol (20 mg/kg bw) pretreatment significantly (p  lessThan  0.05) downregulated the expression of inflammatory markers which have been modified by Fe-NTA. We found that, the renal protective effect of β-sitosterol is associated with the inhibition of the inflammatory cascade through the down regulation of NF-κB activation, TNF-α, iNOS and COX-2 production. Antiinflammatory property of β- sitosterol could provide the link to understand its chemopreventive mechanism in experimental carcinogenesis.</abstract>
<authors>R. SHARMILA, G. SINDHU</authors>
<keywords>Fe-NTA, Inflammatory cascade, NF-ÎºB, Î²-sitosterol.</keywords>
<pages>760-766</pages>
</article>
</Journal>
