• Biotechnology and Bioprocess Engineering:BBE
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• v.5 no.5
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• pp.313-319
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• 2000

A crucial and causative role in the pathogenesis of atherosclerosis is believed to be the oxidative modification of low density lipoprotein (LDL). The oxidation of LDL involves released free radical driven lipid peroxidation. Several lines of evidence support the role of oxidized LDL in atherogenesis. Epidemiologic studies have demonstrated an association between an increased intake of dietary antioxidant vitamins, such as vitamin E and vitamin C and reduced morbidity and mortality from coronary artery diseases. It is thus hypothesized that dietary antioxidants may help prevent the development and progression of atherosclerosis. The oxidation of LDL has been shown to be reduced by antioxidants, and, in animal models, improved antioxidants may offer possibilities for the prevention of atherosclerosis. The results of several on going long randomized intervention trials will provide valuahle information on the efficacy and safety of improved antioxidants in the prevention of atherosclerosis. This review a evaluates current literature involving antioxidants and vascular disease, with a particular focus on the potential mechanisms.

• 한국생물공학회:학술대회논문집
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• 2001.11a
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• pp.800-807
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• 2001

This study was designed to investigate the antioxidative activity of a substance isolated from. The antioxidative activity of procyanidine was higher than that of dl-tocopherol and BHA on low-density lipoprotein (LDL) oxidation by thiobarbituric acid reactive substance (TBARS). Procyanidine inhibited the copper-mediated oxidation of human LDL in a dose dependent manner with almost complete inhibition at $60{\mu}g/mL$. Procyanidine at a concentration of $80{\mu}g/mL$ in hibited oxidation of LDL induced by J774. LDL oxidized by copper-mediated or cell-induced oxidation was degraded at a much greater rate than native LDL. These results suggested the importance of further research to procyanidine in the investigation of atherosclerosis and free radical-induced injury.

• Korean Journal of Pharmacognosy
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• v.27 no.3
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• pp.267-273
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• 1996

The methanol extract of Taraxacum coreanum Nakai (Compositae) was examined on the in vitro oxidation of human low density lipoprotein (LDL). It is well known that LDL oxidation induced artherosclerosis, if we can protect LDL oxidation process, excess plasma lipoprotein accumulation into the arterial lesion prone areas can be blocked. The methanol extract was treated with oxidized LDL which was incubated with $16\;{\mu}M$ $Cu^{2+}$ for metal catalyzed oxidation and TBA value, mobility on agarose gel and formation of conjugated diene and change of vitamin E were determined for the evaluation. The extract showed antioxidative effect at concentration $200\;{\mu}g/ml$ on LDL oxidation.

• Journal of Nutrition and Health
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• v.36 no.9
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• pp.933-941
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• 2003

It has been suggested that green juice supplementation may have some health promoting benefits. We evaluated the effects of green juice (Angelica keiskei) consumption on parameters of lipid profiles and plasma antioxidant status in healthy male smokers. Fifty-four smokers were supplemented with 300 ml of green juice for 6 weeks while maintaining their normal diet. Blood samples were collected on week 0 and week 6 in order to evaluate plasma lipid profiles (total cholesterol, triglyceride, LDL-cholesterol, HDL-cholesterol) , plasma antioxidant vitamin levels (ascorbic acid, $\alpha$ -tocopherol, ${\gamma}$ -tocopherol, $\alpha$ -carotene, $\beta$ -carotene, cryptoxanthin and lycopene) , the degree of LDL oxidation and GOT, GPT levels for liver function. Plasma ascorbic acid level remained at the same level. However, $\alpha$ -tocopherol and ${\gamma}$ -tocopherol normalized by total cholesterol (p <0.05) and $\beta$ -carotene (p <0.001) level were all significantly increased after green juice supplementation. Plasma cholesterol was reduced for 12%, LDL-cholesterol was reduced for 9.3% after green juice consumption, while plasma triglyceride and HDL-cholesterol was not changed. Oxidized LDL assessed by conjugated diene (CD) , was decreased (p < 0.0001) after green juice consumption. These results further support a role for green juice supplementation in the improvement of lipid status, prevention of lipid peroxidation, and thereby reducing risk factors of numerous diseases associated with elevated oxidative stress in smokers.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.269.2-270
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• 2002

Atherosclerosis is a main cause of cardiovascular diseases (that is angina. hypertension. cardiac infarction) and stroke. High level of low-density lipoproteins (LDL) in blood has been implicated as an important factor of atherosclerosis progression. Recently researches in endothelial cells unveiled the roles of Iysophosphatidylcholine (LPC). a constituent of oxidized LDL in atherosclerosis. (omitted)

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

• Journal of Nutrition and Health
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• v.43 no.2
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• pp.123-131
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• 2010

This study was performed to examine the combined effects of gamma linolenic acid and isoflavone supplementation on menopausal symptoms and serum lipids in 73 postmenopausal women. A total subjects were randomly assigned to isoflavone (30 mg) + gamma-linolenic acid (110 mg) group or placebo group. We measured menopausal symptoms by modified Kupperman Index (KI) and oxidized LDL, lipid peroxides, blood components and anthropometric parameters before and after the 12 week intervention period. After the 12 weeks of supplementation, supplement group and placebo group showed a significant reduction of modified kupperman index (p < 0.001). Isoflavone (30 mg) + gamma-linolenic acid (110 mg) supplement group showed a significant reduction of oxidized LDL cholesterol concentration (p = 0.006) whereas placebo group did not show significant change. Isoflavone and gamma-linolenic acid consumption did not significantly affect plasma concentrations of total, LDL, HDL cholesterol, triglyceride, apo A1, B and blood components. The result of present study demonstrated the supplementation of 30 mg isoflavone and 110 mg gamma-linolenic acid per day for 12 weeks may protect LDL cholesterol from oxidative stress.

• Journal of Microbiology and Biotechnology
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• v.32 no.11
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• pp.1406-1415
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• 2022

The formation of macrophage foam cells stimulated by oxidized low-density lipoprotein (ox-LDL) is deemed an important cause of atherosclerosis. Transcription factor Yin Yang 1 (YY1), which is a universally expressed multifunctional protein, is closely related to cell metabolism disorders such as lipid metabolism, sugar metabolism, and bile acid metabolism. However, whether YY1 is involved in macrophage inflammation and lipid accumulation still remains unknown. After mouse macrophage cell line RAW264.7 cells were induced by ox-LDL, YY1 and proprotein convertase subtilisin/kexin type 9 (PCSK9) expressions were found to be increased while low-density lipoprotein receptor (LDLR) expression was lowly expressed. Subsequently, through reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blot analysis, Oil Red O staining and cholesterol quantification, it turned out that silencing of YY1 attenuated the inflammatory response and lipid accumulation in RAW264.7 cells caused by ox-LDL. Moreover, results from the JASPAR database, chromatin immunoprecipitation (ChIP) assay, luciferase reporter assay and Western blot analysis suggested that YY1 activated PCSK9 by binding to PCSK9 promoter and modulated the expression of LDLR in the downstream of PCSK9. In addition, the results of functional experiments demonstrated that the inhibitory effects of YY1 interference on ox-LDL-mediated macrophage inflammation and lipid accumulation were reversed by PCSK9 overexpression. To sum up, YY1 depletion inhibited its activation of PCSK9, thereby reducing cellular inflammatory response, cholesterol homeostasis imbalance, and lipid accumulation caused by ox-LDL.

• The Korean Journal of Food And Nutrition
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• v.24 no.1
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• pp.1-11
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• 2011

This study was designed to investigate the relationships among blood lipid levels, nutrient intakes, oxidation and inflammation markers of overweight adults(23$\leq$BMI<25) and obese(BMI$\geq$25) in Korea. The subjects were classified as control, borderline hyperlipidemia. and hyperlipidemia groups based on The Korean Guidelines of Hyperlipidemia Treatment for the Prevention of Atherosclerosis. The study was conducted through questionnaires, anthropometric checkups, 2-days of 24 hr recalls, and blood biomarker analyses. Systolic blood pressure(SBP) was significantly increased in the hyperlipidemia group(p=0.0464). Intakes of nutrients were not significantly different among the three groups. Blood oxidized-LDL levels were significantly increased in the hyperlipidemia group(p<0.0001). Blood triglyceride(TG) levels were positively associated with BMI(p=0.0498), SBP(p=0.0158), and diastolic blood pressure(DBP; p=0.0076). Blood total cholesterol levels were positively associated with SBP(p=0.0005), and blood HDL-cholesterol levels were negatively associated with body fat (p=0.0408). Blood LDL-cholesterol levels were negatively associated with height(p=0.0207), and blood VLDL-cholesterol levels were positively associated with SBP(p=0.0011) and DBP(p=0.0490). Intakes of protein(p=0.0257) and dietary fiber (p=0.0094) were positively associated with blood HDL-cholesterol levels. Frap levels were positively associated with TG levels(p=0.0001) and VLDL-cholesterol levels(p=0.0077). Oxidized-LDL levels were positively associated with LDL-cholesterol levels(p=0.0135). These results suggest that oxidation and inflammation markers may be related to hypercholesterolemia progress, and dietary fiber intake may play a role in preventing hyperlipidemia in overweight and obese adults.