Abstract
The high prevalence of cardiovascular morbidity and  mortality caused by complication of atherosclerosisneeds an optimal effort to prevent the atherosclerosis progression and complication. Atherogenesis is a chronicinflammatory process which could be prevented via the inhibitionof NFκB, a known key transcription factor involved in inflammatory process. An active component of honeybee hives, CAPE (Caffeic Acid Phenethyl Ester), is believed to inhibit inflammatory process via the inhibition of NFκB activation. However, it remains uncertain whetherCAPE inhibits NFκB activation in endothelial cells. This study therefore was aimed to examine the molecular mechanism of CAPE mediated NFκB inactivation in OxLDL-treated HUVEC’s. Immunohistochemistry using p50 antibody was applied to detectthe migration of NFκB (p50-p65 complex) from inactive form in cytoplasmto active form in nucleus.
Highlights
The high prevalence of cardiovascular morbidity and mortality caused by complication of atherosclerosis needs an optimal effort to prevent the atherosclerosis progression and complication
This study was aimed to examine the molecular mechanism of CAPE mediated
Immunohistochemistry using p50 antibody was applied to detect the migration of NFκB (p50-p65 complex) from inactive form in cytoplasm to active form in nucleus
Summary
The high prevalence of cardiovascular morbidity and mortality caused by complication of atherosclerosis needs an optimal effort to prevent the atherosclerosis progression and complication. NFκB adalah faktor transkripsi yang merangsang proses keradangan dan proliferasi sel kanker, maka kemungkinan efek kerja dari CAPE ini melalui penghambatan aktifasi Tujuan dari penelitian ini adalah untuk menguji apakah CAPE dapat menghambat aktifasi NF B pada sel endotel (Human Umbilical Vein Endothelial Cells=HUVEC’s) yang dipapar oleh OxLDL.
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