• Proceedings of the PSK Conference
• /
• 2003.04a
• /
• pp.141.2-141.2
• /
• 2003

Subendothelial accumulation of foam cells plays a key role in the initiation of atherosclerosis. These foam cells accumulate in fatty streaks that evolve to more complex fibrofatty or atheromatous plaques. Oxidized LDL may also be involved in atherogenesis by inducing smooth muscle cell proliferation and smooth muscle foam cell generation. (omitted)

• The Journal of the Korea Contents Association
• /
• v.12 no.10
• /
• pp.349-356
• /
• 2012

In the diagnosis of coronary artery atheromatous plaque, Cardiac computed tomography (Cardiac Computed Tomographic Angiography: CCTA) compared with IVUS(Intravascular Ultrasound: IVUS) investigate the diagnostic accuracy, Interested in CCTA atheromatous plaque in computed tomography values (Hounsfield Unit: HU) try to find out. From April 2006 to August 2008 among coronary artery disease(Coronary Artery Disease: CAD) patients with confirmed or suspicious of CAD by CCTA performed atherosclerotic plaques and found 200 patients who underwent IVUS were enrolled. 200 patients who underwent CCTA and IVUS results from the 476 plaque was found, IVUS results of the soft plaque(n; 84), fibrous plaque(n; 63), mixed plaque (n; 97), calcific plaque(n; 232). The results are classified according to the IVUS plaque in HU in the soft plaque : $53.8{\pm}10.5$, fibrous plaque : $108.1{\pm}20.0$, mixed plaque : $371.2{\pm}113.1$, and calcific plaque : $731.0{\pm}160.4$. CCTA had sensitivity of 97% and confidence interval of 95.0-98.3. This study that is the diagnosis of coronary atheromatous plaque for using CCTA, we confirm the high sensitivity and the confidence interval Based on IVUS results CCTA atheromatous plaque with HU in the analysis could be classified to characterize in the treatment of patients with CAD is expected to help.

• Journal of Yeungnam Medical Science
• /
• v.21 no.2
• /
• pp.143-150
• /
• 2004

A thromboembolic stroke is believed to be precipitated by a rupture of vulnerable atheromatous plaques. Until recently the assessment of a further risk of stroke in high-risk patients in whom atherosclerosis has presented with a transient ischaemic attack (TIA), has been confined to a quantitative assessment of the luminal patency of the internal carotid artery. These traditional stratification parameters are no longer believed to be the most accurate predictors of a thrombo-embolism. This is because the process of vessel wall remodeling can maintain a luminal patency, and consequently, quite large friable plaques may remain unidentified. Accordingly, there is a need for an improved risk assessment. The fibrous cap of a vulnerable plaque is thinner, and an intraplaque hemorrhage and inflammation can occur during the development of atherosclerotic plaque. Several imaging methods for identifying vulnerable plaques have been developed. Recently, high resolution magnetic resonance (MR) imaging has emerged as an accurate non-invasive tool that can characterize the carotid plaque components in vivo. A High resolution carotid magnetic resonance is capable of distinguishing an intact, thick fibrous cap from a thin and ruptured cap in carotid plaque. In addition, a plaque MR can identify the active inflammation and detect a hemorrhage. High resolution carotid MR imaging is a valuable noninvasive method for quantifying the plaque components and identifying vulnerable plaque.

• Biomolecules & Therapeutics
• /
• v.19 no.3
• /
• pp.302-307
• /
• 2011

Peptidoglycan (PGN) is detected in inflammatory cell-rich regions of human atheromatous plaques. The present study investigated the effects of PGN on CC chemokine ligand 3 (CCL3) expression, which is elevated in the atherosclerotic arteries, and determined cellular factors involved in PGN-mediated CCL3 up-regulation in mononuclear cells, with the goal of understanding the molecular mechanisms of inflammatory responses to bacterial pathogen-associated molecular patterns in diseased arteries. Exposure of human monocytic leukemia THP-1 cells to PGN resulted in enhanced secretion of CCL3 and profound induction of the CCL3 gene transcript. Both events were abrogated by oxidized 1-palmitoyl-2-arachidonosyl-sn-phosphatidylcholine, an inhibitor of Toll-like receptors 2/4. Pharmacological inhibitors such as U0126, SP6001250, Akt inhibitor IV, rapamycin, RO318220, diphenyleneiodonium chloride, and N-acetylcysteine also significantly attenuated PGN-mediated CCL3 up-regulation. However, polymyxin B, LY294002, and SB202190 did not influence CCL3 expression. We propose that PGN contributes to enhanced CCL3 expression in atherosclerotic plaques and that Toll-like receptors (TLR2), Akt, mTOR, mitogen-activated protein kinase, and reactive oxygen species are involved in that process.

• YAKHAK HOEJI
• /
• v.44 no.1
• /
• pp.71-79
• /
• 2000

Curcumin, the yellow pigment in turmeric, curry and mustard, has anti-inflammatory and anti-carcinogenic activities. In this study; we investigated the hypocholesterolemic and anti-atherogenic effect of curcumin in rabbits. Hypercholesterolemia was induced by feeding high cholesterol diet to male rabbits for 30 days, and the animals were then fed high cholesterol diet containing 0.1% (w/w) or 0.5% (w/w) curcumin for additional 30 days. Supplementation of 0.l% curcumin tended to lower serum total cholesterol and low density lipoprotein (LDL)-cholesterol levels and inhibit serum lipid peroxidation. In the 0.5% curcumin-supplemented group, serum total cholesterol was significantly lowered by 11.7%, LDL-cholesterol by 12.8% and lipid peroxidation by 47.9% compared to the control group. Hepatic cholesterol and triglyceride contents were also significantly lowered by 50.6% and 37.4%, respectively compared to the control group. Lipid staining of the arteries isolated from the curcumin-treated rabbits showed that curcumin significantly decreased formation of fatty streaks and atheromatous plaques on the intima of the arteries. These results demonstrated that curcumin lowered serum cholesterol concentration, hepatic cholesterol and triglyceride contents, and accumulation of cholesterol in the artery These cholesterol lowering effects of curcumin, together with its anti-oxidative and anti-inflammatory activities, may play some important roles in preventing atherosclerosis.

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.5
• /
• pp.591-600
• /
• 1998

We have examined 24 human aortas aged $46{\sim}90$ years obtained from autopsies. Most exhibited gross lesions of some degree on the lumenal surface. Using hot alkaline treatment (0.1 N NaOH) at $70{\sim}75^{\circ}C$ for 5 hours, we extracted and quantitated elastin portions from the aortic wall in 3 different segments (UTA=upper thoracic aorta, LTA=lower thoracic aorta, AA=abdominal aorta). We have found UTA had $70.6%{\pm}1.39$ (SE), LTA $61.6%{\pm}1.94$ (SE), AA $49.2%{\pm}1.84$ (SE) elastin respectively based on wet weight. The differences between segments are statistically significant (p＜0.05, 0.025). However, there is no significant correlation between the age of the patients and the relative amounts of elastin in each segment. We have also observed the structure of elastin in the internal elastic lamina (IEL) and tunica media (TM) with SEM (scanning electron microscopy), and discovered that the IEL shows various forms of elastolysis- broken sheets, discontinuity, various sizes of lumps, vesicles, and possible newly formed elastin in the aortic lesions (Song and Roach submitted to YMJ). From these studies we conclude that elastin in the aortic wall remains well balanced quantitatively with age in spite of evidence suggesting vigorous degeneration and regeneration in the atherosclerotic lesions.

• Korean Journal of Pharmacognosy
• /
• v.31 no.2
• /
• pp.149-156
• /
• 2000

Atherosclerosis is emerging as one of the major causes of death in Korea as well as Western societies. In the present study; hypocholesterolemic and antiatherogenic effects of the ethanol extract of Allium victorialis Makino was investigated using the conventional rabbit and the cholesteryl ester transfer protein (CETP)-transgenic mouse model. Hypercholesterolemia was induced by feeding high cholesterol diet to the animals for 30 days and they were then fed with high cholesterol diet containing 0.5% of the A. victorialis extract for additional 30 (or 40) days. In the experiment using rabbits, treatment with the A. victorialis extract significantly decreased plasma total cholesterol, low density lipoprotein (LDL)-cholesterol, triglyceride levels and lipid peroxidation compared to those in the control group. Total cholesterol contents in the liver and the heart were also significantly decreased. Lipid staining of the aorta isolated from the rabbits showed that treatment with the A. victorialis extract decreased formation of atheromatous plaques on the intima of the aorta. In the experiment employing CETP transgenic mouse model, treatment with the A. victorialis extract decreased the levels of plasma total cholesterol and the tissue triglyceride levels in the heart. These results demonstrated that the ethanol extract of A. victorialis lowered serum cholesterol levels, tissue lipid contents and accumulation of cholesterol in the artery.

• Journal of Life Science
• /
• v.32 no.6
• /
• pp.421-429
• /
• 2022

The expression of interleukin-1α (IL-1α) is elevated in monocytic cells, such as monocytes and macro-phages, within atherosclerotic arteries, yet the cellular molecules involved in cytokine upregulation remain unclear. Because peptidoglycan (PG), a major component of gram-positive bacterial cell walls, is detected within the inflammatory cell-rich regions of atheromatous plaques, it was investigated if PG contributes to IL-1α expression in monocytes/macrophages. Exposure of THP-1 monocytic cells to PG resulted in elevated levels of IL-1α gene transcripts and increased secretion of IL-1α protein. The transcription and secretion of IL-1α were abrogated by OxPAPC, an inhibitor of TLR2/4, but not by polymyxin B that inhibits lipopolysaccharide-induced TLR4 activation. To understand the molecular mechanisms of the inflammatory responses due to bacterial pathogen-associated molecular patterns (PAMPs) in diseased arteries, we attempted to determine the cellular factors involved in the PG-induced upregulation of IL-1α expression. Pharmacological inhibition of cell signaling pathways with LY294002 (a PI3K inhibitor), Akti IV (an inhibitor of Akt activation), rapamycin (an mTOR inhibitor), U0126 (a MEK inhibitor), SB202190 (a p38 MAPK inhibitor), SP6001250 (a JNK inhibitor), and DPI (a NOX inhibitor) also significantly attenuated the PG-mediated expression of IL-1α. These results suggest that PG induces the monocytic or macrophagic expression of IL-1α, thereby contributing to vascular inflammation, via multiple signaling molecules, including TLR2, PI3K/Akt/mTOR, and MAPKs.