• Journal of the Korean Dietetic Association
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• v.4 no.1
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• pp.20-29
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• 1998

The purpose of this study was to investigate the effect of food habits on blood components level(blood glucose, uric acid, hemoglobin, some lipids levels) and health condition in Taejon. The study was conducted with 250 subjects (male 130, female120) who visited in a general hospital from May to June in 1997. Questionaires were used for food habits. The data were analyzed by using $x^2$-test, t-test, ANOVA and multiple range test. Results were summerized s follow : mean of Broca Index were 110.0 $\pm$13.7% in male, 110.6$\pm$16.6% in female. Mean values of systolic blood pressure and diastolic blood pressure were 130.9$\pm$17.6mmHg, 76.2$\pm$12.6mmHg, respectively. The systolic blood pressure was significantly higher in man than woman, Mean serum total cholesterol, LDL-cholesterol, and HDL-cholesterol and triglyceride levels were 202.8$\pm$40.2, 121.1$\pm$35.5, 50.3$\pm$12.9, 157.1$\pm$112.6mg/dl, respectively. Triglyceride level was significantly higher in man than woman. But HDL-cholesterol was significantly lower in man than woman. And also, the value of LPH and AI were higher in man. So Man has more risk of atherogenesis than woman. Mean values of blood sugar, uric acid and hemoglobin was 102.7$\pm$1.36mg/dl and 14.1$\pm$1.56g/dl were higher in man than woman except blood sugar. Food habit of woman were better than it of man. The levels of education and income did not affect to food habit score. The most problem of habits were intake of salty food and lack of exercise. The intake of nutrients were higher as food habit score was higher. Intakes of energy, Ca, vitamin A and vitamin $B^1$ were lower than RDA's of nutrients in bad food habit group. This result did not show that blood components level and health condition were significantly different by food habits. But Broca Index and triglyceride levels were higher in bad food habit group than other groups, but not statistically significant. By this result, it is more needed food habit education to man and young people. The education of food habits will include the real methods of weight control, low intake of salt and exercise to bad food habit group.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.6
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• pp.1652-1660
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• 2004

Apoptosis of vascular smooth muscle cells(VSMCs) is essential in atherogenesis, being a factor that modulates its early progression rather than a terminal event in the course of the disease. Various stimuli, including oxide lipoproteins, altered hemodynamic stress and free radical, can induced VSMCs apoptosis in vitro. The protective effects of Sophorae Radix (SR) on apoptotic cell death induced by H₂O₂ were investigated in VSMCs. The viability of VSMCs was markedly decreased by H₂O₂. Sophorae Radix protected the H202-induced apoptotic death of VSMCs, which was characterized as nuclear fragmentation and increase of sub-G0/G1 fraction .. Sophorae Radix decreased the activation of caspase-3 like protease induced by H₂O₂ and recovered control level from H202-induced PARP, Bak, Bcl-XL and mitochondrial membrane potential. These results suggest that Sophorae Radix protected VSMCs apoptotic death induced by H₂O₂ via inactivation of caspase-3 and modulation of mitochondrial function. Also, the expression profile of proteins by using two-dimensional (2-D) gel electrophoresis was screened. Future investigations will need to explore the use of an anti atherosclerotic therapy of Sophorae Radix, which relies on inhibition of the proapoptotic activation of the vascular smooth muscle cells.

• Journal of Nutrition and Health
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• v.36 no.9
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• pp.908-917
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• 2003

It has been proposed that oxidative modification of LDL (oxLDL) plays a significant role in the pathogenicity of atherogenesis. We tested the hypothesis that chitin and chitosan may function as antioxidants with respect to 0.1 mg cholesterol/ml LDL incubated with 5 $\mu$ M Cu$^2$$^{+}$alone or in the P338Dl mouse macrophage system using L-ascorbic acid as a standard classical antioxidant. The degree of oxLDL formation was ascertained by the relative electrophoretic mobility (rEM) in the combination of thiobarbituric acid reactive substances (TBARS) levels, and the cytotoxicity of oxLDL was detected by macrophage viability. The oxLDL uptake and foam cell formation of macrophages were measured by Oil Red O staining. Incubation with Cu$^2$$^{+}$and macrophages increased rEM of LDL and stimulated TBARS formation. Culture of macrophages with LDL in the presence 5 $\mu$ M Cu$^2$$^{+}$induced macrophage death. In cell-free system 200 $\mu$g/ml water-soluble chitosan and chitosan-oligosaccharide blocked oxLDL formation. Water-soluble chitosan and chitosan-oligosaccharide blocked oxLDL formation near-completely relative to L-ascorbic acid, whereas water-soluble chitin and chitin-oligosaccharide had no measurable antioxidant effect. In macrophage system water-soluble chitosan and chitosan-oligosaccharide blocked oxidation of LDL with a significant increase in cell viability, and decreased TBARS in medium. As for the inhibitory effect on macrophage foam cell formation, chitosan and its oligosaccharide, but not watersoluble chitin, revealed the effectiveness. The endothelial expression of lectin-like oxLDL receptor-1 (LOX-1) was tested by Western blot analysis, and chitosan, chitosan-oligosaccharide and chitin-oligosaccharide blocked LOX-1 expression. These results indicate that water-soluble chitosan and its oligosaccharide showed the inhibitory effect on Cu$^2$$^{+}$-induced LDL oxidation of macrophages, and chitosan, chitosan-oligosaccharide and chitin-oligosaccharide had blocking effect on oxLDL receptor expression in the human umbilical vein endothelial system. Thus, water-soluble chitosan and its oligosaccharides possess anti-atherogenic potentials possibly through the inhibition of macrophage LDL oxidation or endothelial oxLDL receptor expression depending on chemical types.l types.

• Nutrition Research and Practice
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• v.12 no.5
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• pp.371-377
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• 2018

BACKGROUND/OBJECTIVES: Elevation of postprandial lipemia characterized by a rise in triglyceride (TG)-rich lipoproteins can increase the risk of atherogenesis. The objective of this study was to investigate postprandial lipemia response to a single dietary fat/sugar load test and monitor beneficial changes induced by the consumption of Platycodi radix (AP) beverage in healthy subjects. SUBJECTS/METHODS: A total of 52 subjects were randomly assigned to either placebo or AP beverage group with a high-fat shake in a randomized controlled crossover trial. Postprandial blood was collected at 0, 1, 2, 4, and 6 h and analyzed for TG and lipoprotein lipase mass. Inhibition of pancreatic lipase was determined in vitro. RESULTS: AP inhibited pancreatic lipase activity in vitro ($IC_{50}=5mg/mL$). Compared to placebo beverage, AP beverage consumption with a high-fat shake induced significant increase of plasma lipoprotein lipase mass (P = 0.0111, ${\beta}$ estimate = 4.2948) with significant reduction in very low-density lipoprotein (VLDL) TG concentration (P = 0.038, ${\beta}$ estimate = -52.69) at 6 h. Based on significant correlation between high-fat dietary scores MEDFICTS and postprandial TG responses in VLDL (P = 0.0395, r = 0.2127), subgroup analysis revealed that 6 h-postprandial VLDL TG response was significantly decreased by AP consumption in subjects with MEDFICTS ${\geq}40$ (P = 0.0291, ${\beta}$ estimate = -7214). CONCLUSIONS: AP beverage might have potential to alleviate postprandial lipemia through inhibiting pancreatic lipase activity and elevating lipoprotein lipase mass. Subgroup analysis revealed that subjects with high-fat dietary pattern could be classified as responders to AP beverage among all subjects.

• Journal of Life Science
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• v.14 no.1
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• pp.180-187
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• 2004

Crowing evidence indicates that oxidized low density lipoprotein (LDL) nay promote atherogenesis. Therefore, inhibition of LDL oxidation may impede this process. The effect of geraniin on the susceptibility of human low density lipoprotein (LDL) to macrophages-induced oxidation was investigated by monitoring a thiobarbiruric acid reactive substrance (TBARS). The antioxidative activity of geraniin was higher than that of $\alpha$-tocopherol on low density lipoprotein (LDL) oxidation by thiobarbituric acid reactive substance (TBARS). Geraniin inhibited the C $u^{2+}$ mediated oxidation of human LDL in a dose dependent manner at concentration of 50 and 100 $\mu\textrm{g}$/mL. Geraniin, almost completely inhibited the macrophages mediated LDL oxidation in electrophoretic mobility and conjugate diene of LDL oxidation. Also, geraniin almost completely inhibited 0$_2$$^{[-10]}$ at concentration of 100 $\mu\textrm{g}$/mL. The physiological relevance of the antioxidative activity was validated at the cellular level where geraniin inhibited endothelial cell mediated LDL oxidation, When compound with several other antioxidants geraniin showed a high activity equal to natural antioxidants, $\alpha$-tocopherol and ascorbic acid, and the synthetic antioxidant, protocol. These results indicate that geraniin might play a protective antioxidant effects on LDL, probably affecting both the structural properties of macrophage and endothelial cell for the LDL oxidation..

• Journal of Food Hygiene and Safety
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• v.22 no.1
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• pp.1-14
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• 2007

The term, "food safety", has traditionally been viewed as a practical science aimed at assuring the prevention acute illnesses caused by biological microorganisms, and only to a minor extent, chronic diseases cause by chronic low level exposures to natural and synthetic chemicals or pollutants. "food safety" meant to prevent microbiological agents/toxins in/on foods, due to contamination any where from "farm to Fork", from causing acute health effects, especially to the young, immune-compromised, genetically-predisposed and elderly. However, today a broader view must also include the fact that diet, perse (nutrients, vitamins/minerals, calories), as well as low level toxins and pollutant or supplemented synthetic chemicals, can alter gene expressions of stem/progenitor/terminally-differentiated cells, leading to chronic inflammation and other mal-functions that could lead to diseases such as cancer, diabetes, atherogenesis and possibly reproductive and neurological disorders. Understanding of the mechanisms by which natural or synthetic chemical toxins/toxicants, in/on food, interact with the pathogenesis of acute and chronic diseases, should lead to a "systems" approach to "food safety". Clearly, the interactions of diet/food with the genetic background, gender, and developmental state of the individual, together with (a) interactions of other endogenous/exogenous chemicals/drugs; (b) the specific biology of the cells being affected; (c) the mechanisms by which the presence or absence of toxins/toxicants and nutrients work to cause toxicities; and (d) how those mechanisms affect the pathogenesis of acute and/or chronic diseases, must be integrated into a "system" approach. Mechanisms of how toxins/toxicants cause cellular toxicities, such as mutagenesis; cytotoxicity and altered gene expression, must take into account (a) irreversible or reversal changes caused by these toxins or toxicants; (b)concepts of thresholds or no-thresholds of action; and (c) concepts of differential effects on stem cells, progenitor cells and terminally differentiated cells in different organs. This brief Commentary tries to illustrate this complex interaction between what is on/in foods with one disease, namely cancer. Since the understanding of cancer, while still incomplete, can shed light on the multiple ways that toxins/toxicants, as well as dietary modulation of nutrients/vitamins/metals/ calories, can either enhance or reduce the risk to cancer. In particular, diets that alter the embryo-fetal micro-environment might dramatically alter disease formation later in life. In effect "food safety" can not be assessed without understanding how food could be 'toxic', or how that mechanism of toxicity interacts with the pathogenesis of any disease.

• The Korean Journal of Blood Transfusion
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• v.29 no.3
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• pp.229-239
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• 2018

The circulatory system is closely related to the inter-relationship between the anatomy of the heart and blood vessels, and the fluid dynamic properties of blood. The physical properties of blood, which affect blood flow, are called hemorheologic factors. Hemorheologic factors, such as blood viscosity and erythrocyte aggregation, are influenced mainly by hematocrit. A higher hematocrit level results in an increase in blood viscosity, erythrocyte aggregation, which impedes the circulation itself, and tissue oxygenation. An excess of serum ferritin causes injury to vascular endothelial cells and erythrocytes via oxygen free radicals. In addition, an excess of blood can aggravatee the adverse effects of the hemorheologic parameters and induce atherogenesis, microcirculatory disturbances, and major cardiovascular events. A preventive and therapeutic approach with a phlebotomy or blood donation has been stimulated by the knowledge that blood loss, such as regular donations, is associated with significant decreases in key hemorheologic variables, including blood viscosity, erythrocyte aggregation, hematocrit, and fibrinogen. Major cardiovascular events have been improved in regular blood donors by improving blood flow and microcirculation by decreasing the level of oxidative stress, improving the hemorheologic parameters, and reducing the serum ferritin level. Confirmation of the positive preventive and therapeutic effects of blood donations on cardiovascular disease by a well-designed and well-controlled Cohort study may be good news to patients with cardiovascular disease or at risk of these diseases, as well as patients who require a transfusion.

• Nutrition Research and Practice
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• v.17 no.6
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• pp.1099-1112
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• 2023

BACKGROUND/OBJECTIVES: Dyslipidemia causes metabolic disorders such as atherosclerosis and fatty liver syndrome due to abnormally high blood lipids. Purple perilla frutescens extract (PPE) possesses various bioactive compounds such as α-asarone, chlorogenic acid and rosmarinic acid. This study examined whether PPE and α-asarone improved dyslipidemia-associated inflammation and inhibited atheroma formation in apolipoprotein E (apoE)-deficient mice, an experimental animal model of atherosclerosis. MATERIALS/METHODS: ApoE-deficient mice were fed on high cholesterol-diet (Paigen's diet) and orally administrated with 10-20 mg/kg PPE and α-asarone for 10 wk. RESULTS: The Paigen's diet reduced body weight gain in apoE-deficient mice, which was not restored by PPE or α-asarone. PPE or α-asarone improved the plasma lipid profiles in Paigen's diet-fed apoE-deficient mice, and despite a small increase in high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein (LDL)-cholesterol, and very LDL were significantly reduced. Paigen's diet-induced systemic inflammation was reduced in PPE or α-asarone-treated apoE-deficient mice. Supplying PPE or α-asarone to mice lacking apoE suppressed aorta atherogenesis induced by atherogenic diet. PPE or α-asarone diminished aorta accumulation of CD68- and/or F4/80-positive macrophages induced by atherogenic diet in apoE-deficient mice. Treatment of apoE-deficient mice with PPE and α-asarone resulted in a significant decrease in plasma cholesteryl ester transfer protein level and an increase in lecithin:cholesterol acyltransferase reduced by supply of Paigen's diet. Supplementation of PPE and α-asarone enhanced the transcription of hepatic apoA1 and SR-B1 reduced by Paigen's diet in apoE-deficient mice. CONCLUSIONS: α-Asarone in PPE inhibited inflammation-associated atheroma formation and promoted hepatic HDL-C trafficking in dyslipidemic mice.

• Journal of Life Science
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• v.19 no.2
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• pp.289-298
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• 2009

Effects of Nattokinase fibrinol (NKF), defined as a fibrinolytic product, on fibrinolytic and atherogenetic markers were studied for healthy adults (20-31 years old), who is smoking more than 20 cigarettes per day. Subjects were divided into 29 for NKF group and 10 for placebo group in a short term study. They were given 2 tablets of NKF (4,000 unit) or placebo tablet and thereafter blood samples were collected at 0, 2, 4 hr prerid. For a 4-week long term study, 15 subjects for NFK group and 10 subjects for placebo group were supplemented one tablet of each NKF (2,000 unit) and placebo per day, respectively. Blood samples were collected at 0, 1, 2, 4 weeks later. The short-term experimental trial showed that NKF remarkably increased fibrinolytic activity at 2hr after consumption, which was maintained up to 4 hr, relative to that of placebo, while NKF reduced the euglobulin clot lysis time (ECLT) and retarded the activated partial thromboplastin time (aPTT), as compared to placebo group. NKF supplementation for 4 weeks elevated fibrinolytic activity, shortened ECLT and retarded aPTT. Furthermore, NKF supplementation increased anti-atherogenic index by decreasing triglyceride (TG) and elevating high-density lipiprotein (HDL)-cholesterol. These results indicate that NKF supplementation for short term or long term might have beneficial effects on preventing and treating cardiovascular disease by increasing fibrinolytic activity and improving atherogenic markers such as hyperlipidemia.

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.6
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• pp.1134-1141
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• 2002

Adhesion of leukocytes to the activated vascular endothelium and their subsequent recruitment/migration into the artery wall are key features in the pathogenesis of atherosclerosis and inflammatory diseases. These features have been mediated by cell adhesion molecules including vascular cell adhesion molecule-1 (VCAM-1) and in tracellular cell adhesion molecule-1 (ICAM-1). This study examined whether flavonoids inhibit the pro-inflammatory cytokine TNF-$\alpha$-induced monocyte adhesion via a modulation of the protein expression of VCAM-1 and ICAM-1 of human umbilical vein endothelial cells (HUVECs). TNF-$\alpha$ markedly increased the adhesion of THP-1 monocytes to endothelial cells and induced the expression of VCAM-1, ICAM-1 and E-selectin proteins in HUVECs. Micromolar concentrations of the flavones luteolin and apigenin and the flavonol quercetin near completely blocked the monocyte adhesion to the activated endothelial cells and the induction of these adhesion molecules. However, equimicromolar catechins of (-)epigallocatechin gallate and (+)catechin, the flavonol myr- icetin and the flavanones of naringin and hesperidin had no effect on TNF-$\alpha$-activated monocyte adhesion. (-)Epigallocatechin gallate, (+) catechin, and naringin did not attenuate the TNF-$\alpha$ induction of these adhesion molecules. Furthermore, culture with luteolin and apigenin strongly blocked the expression of TNF-$\alpha$-induced VCAM-1 mRNA and modestly attenuated ICAM-1 mRNA. Quercetin modestly decreased the TNF-$\alpha$-activated VCAM-1 and ICAM-1 mRNAs. These results demonstrate that flavonoids classified as flavones and flavonols may inhibit monocyte adhesion to the TNF-$\alpha$-activated endothelium, most likely due to a blockade of expression of functional adhesion molecules down-regulated at the transcriptional level, indicating a definite linkage between the chemical structure of flavonoids and the expression of cell adhesion molecules. Furthermore, the antiathero-genic feature of flavonoids appears to be independent of their antioxidant activity.