TY  - JOUR
T1  - <I>Anacardium occidentale</I> Aqueous Extract Attenuates Hydrogen Peroxide-Induced Oxidative Injury and Inhibits Inflammatory Mediators Expression in TNF-&#945;-Induced Human Umbilical Vein Endothelial Cells During Initial Stage of Atherogenesis
AU - Kamal NH., M. AU - Zulkhairi, A. AU - Hafizah, A.H. AU - Fazali, F. AU - Khairul Kamilah, A.K. AU - Rasadah, M.A. AU - Zamree, M.S. AU - Shahidan, M.A.M. 
JO  - Research Journal of Biological Sciences
VL  - 4
IS  - 12
SP  - 1230
EP  - 1235
PY  - 2009
DA  - 2001/08/19
SN  - 1815-8846
DO  - rjbsci.2009.1230.1235
UR  - https://makhillpublications.co/view-article.php?doi=rjbsci.2009.1230.1235
KW  - Anacardium occidentale
KW  -HUVEC
KW  -antioxidant
KW  -anti-inflammation
KW  -atherogenesis
KW  -atherosclerosis
AB  - Endothelial cell injury due to inflammation and oxidative stress are the hallmark of early pathologic events of atherosclerosis. Antioxidants derived from natural sources have been extensively used to prevent oxidative stress. The purpose of this study was to investigate the cytoprotective effect of <I>Anacardium occidentale</I> Aqueous Extract (AOE) against H<SUB>2</SUB>O<SUB>2</SUB>-induced HUVEC injury and its anti-inflammatory potential induced by TNF-&#945; <I>in vitro</I>. HUVEC was exposed with various concentrations of H<SUB>2</SUB>O<SUB>2</SUB> (0-700 &#956;M) and it was observed that 250 &#956;M of H<SUB>2</SUB>O<SUB>2 </SUB>reduced cell viability by 50% (IC<SUB>50</SUB>) as denoted by MTT assay. Using the above concentration as the PC, the cells were pretreated with AOE at various concentration (50-700 &#956;g mL<SUP>-1</SUP>) for 30 min followed by 24 h incubation with H<SUB>2</SUB>O<SUB>2 </SUB>(250 &#956;M) or TNF-&#945; (10 ng mL<SUP>-1</SUP>), respectively. AOE was found to be not toxic to the cells as no inhibitory concentration (IC<SUB>50</SUB>) obtained. AOE (100-300 &#956;g mL<SUP>-1</SUP>) protects cellular damage and prevent microsomal lipid peroxidation in H<SUB>2</SUB>O<SUB>2</SUB>-induced HUVEC indicated with low MDA levels. The AOE at similar concentrations also suppressed the production of VCAM-1, ICAM-1, MCP-1 and M-CSF in TNF-&#945;-induced inflammation whereas NF-&#954;B p65 translocation into nucleus was observed inactivated. These data suggested that AOE possessed antioxidative properties and attenuate the initial stage of atherogenesis <I>in vitro</I>. Inhibition of NF-&#954;B activation could be the possible underlying mechanism in modulating early events of atherogenesis.
ER  -