Abstract
Background . Atherosclerosis is a chronic inflammation process of vascular endothelial cells. Increased oxydized LDL (OxLDL) is one of the most potent inducer of atherogenesis. OxLDL induces an increased ROS (Reactive Oxigen Species) and also acts as cytotoxic and chemotaxis factor for monocytes result in accumulation of inflammatory cells. Nuclear Factor Kappa Beta (NFkB) is a transcription factor that plays an important role in this inflammatory proces. NFkB compose of heterodimer molecules of p50 and p65, which bind to its inhibitor, IkB, leading to its inactive form in cytoplasm. OxLDL activates NFkB complex by phosphorylate IkB resulting in released p50-p65-IkB binding and translocation of p50-p65 into the nucleus. p50-p65 then binds to promoter and activates transcription of target genes. NFkB activation therefore increase gene and protein expressions of target molecules such TNF-α, ICAM-1, VICAM, etc. This study aimed to examine whether Moringa oleifera inhibits activation of NFkB dan expression of cytokine TNF-α and adhesion molecule ICAM-1. Methods and results . Human umbilical vein endothelial cells (HUVECs) treated with OxLDL were used as model of atherosclerosis. The increased NFkB activity was measured by indirect method using p50 subcellular localization by immunohistochemistry. 40ug/mL OxLDL, 0.01 gr/mL and 0.005 gr/mL Moringa oleifera were used based on preliminary study. Conclusions . This study showed that OxLDL significantly induce NFkB activation and increase protein expression of TNF-α and (ICAM-1). This study also observed that Moringa oleifera significantly inhibit NFkB activation, and prevent an increased TNF-α and ICAM-1 expression at protein level in OxLDL-treated HUVECs as compare to the controls. Moringa oleifera dose of 0.01mg/mL has a better inhibition effect as compare to that of 0.005 gr/mL.
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