• Proceedings of the Korean Society of Food Hygiene and Safety Conference
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• 2002.05a
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• pp.137-137
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• 2002

Several epidemiologidal studies suggested that arsenic exposure was strongly correlated with the development of cardiovascular disease such as hypertension. In order to examine whether arsenic affects vasomotor tone in blood vessels, we investigated the effect of arsenic on agonist-induced vasorelaxation using the isolated rat aortic ring in in vitro organ bath system. Treatment with arsenite inhibited acetylcholine-induced relaxation of aortic rings in a concentration- dependent manner. The inhibitory effects by arsenic were also observed in the relaxation induced by sodium nitroprusside, a NO-donor. Consistent with these findings, the cGMP levels stimulated by acetylcholine in blood vessels were reduced significantly by arsenite treatment. In addition, higher concentration of arsenite decreased the relaxation by 8-Br-cGMP, a cGMP analog, in aortic rings without endothelium. These in vitro results indicated that arsenite that arsenite was capable of suppressing acetylcholine-induced relaxation in blood vessels by inhibiting production of nitric oxide in endothelial cells and by impairing the relaxation machinary in smooth muscle cells. In vivo studies revealed that the reduction of blood pressure by acetylcholine infusion was signigicantly suppressed after arsenite was administered intravenously to rate. These data suggest that vasomotor tone impaired by arsenite exposure may be one of the contrbuting factors in development of cardiovascular disease.

• Journal of Nutrition and Health
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• v.10 no.2
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• pp.5-11
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• 1977

The mature human braun contains over 10 billion nerve cells (neurons), whose functions are directly related to the acquisition, transfer, processing, analysis, and utilization of all the information. There are also billions of glial cells, which serve primarily to support and to maintain the integrity of the neuron network and to synthesize an essential fatty strucfure, myelin. In the human brain DNA content therefore cell number rises rapidly until birth and then more slowly until $5{\sim}6$ months of age, when it reaches a maximum. While glial cells may be replaced, the more important nerve cell neurons can never be replaced once they are formed. Humans are born with their full complement of neurons and every neuron is as old as each individual. Thus prenatal malnutrition can seriously affect a person's entire life by severely inhibiting the production of neurons before birth.It has been demonstrated that in humans severe malnutrition during the fetal period and in infancy is associated with intellectual impairment. Severely malnourished children have brains smaller than average size and have been found to have $15{\sim}20%$ fewer brain cells than wellnourished childen. There is growing body of literature pointing to malnutrition as a cause of abnormal behavior as evidence that suggests these abnormalities may produce chromosomal damage that may persist forever. Although cognitive development in children is affected by multiple environmental factors, nutrition certainly deaerves more attention than it has received.

• BMB Reports
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• v.47 no.9
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• pp.524-529
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• 2014

Oxidative stress and inflammation are common to many pathological conditions. Defense mechanisms protect cells from oxidative stress, but can become over-activated following injury and inflammation. NF-${\kappa}B$ and Nrf2 transcription factors regulate proinflammatory and antioxidant gene expression, respectively. Studies have shown that many natural dietary compounds regulate NF-${\kappa}B$ and Nrf2, preventing inflammation and oxidative stress. Here, we report major compounds of Prunella vulgaris var. lilacina such as rosmarinic acid, oleanolic acid, ursolic acid and caffeic acid as a potential therapeutic for oxidative stress and inflammation. The major compounds exhibited high anti-inflammatory activity, inhibiting NO, PGE2 production, NF-${\kappa}B$ expression and activating Nrf2 expression. In addition, we examined the effect of major compounds on MafK expression. Among the compounds, oleanolic acid significantly decreased MafK expression and MafK-mediated p65 acetylation. These findings suggest that oleanolic acid as NF-${\kappa}B$ inhibitors can potentially be used in therapeutic applications for the treatment of oxidative stress-induced diseases.

• Natural Product Sciences
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• v.17 no.4
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• pp.273-278
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• 2011

In this study, the effects of a methanol (MeOH) extract of Carduus crispus L. (Asteraceae) on adipogenesis was investigated in 3T3-L1 cells. To differentiate preadipocytes to adipocytes, confluent 3T3-L1 preadipocytes were treated with a hormone mixture, which included isobutylmethylxanthine, dexamethasone, and insulin (MDI). The methanol extract of C. crispus significantly decreased fat accumulation by inhibiting adipogenic signal transcriptional factors in MDI-induced 3T3-L1 cells in a dose-dependent manner. In MTT assays and on PI-staining, methanol extract of C. crispus inhibited the proliferation of 3T3-L1 cells during mitotic clonal expansion (MCE). The anti-adipogenic effect of the Carduus extract seemed to be associated with the upregulation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) pathways within the first 2 days after MDI treatment. These results suggest that methanol extract of C. crispus might be beneficial for the treatment of obesity.

• Natural Product Sciences
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• v.26 no.3
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• pp.221-229
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• 2020

This study was undertaken to investigate the protective effect of rice bran oil (RBO) on amyloid β protein (Aβ) (25-35)-induced memory impairment and brain damage in an ICR mouse model. Memory impairment was produced by intracerebroventricular microinjection of 15 nmol Aβ (25-35) and assessed using the passive avoidance test. Treatment with RBO at 0.1, 0.5, or 1 mL/kg (p.o. daily for 8 days) protected against Aβ (25-35)-induced memory impairment. Furthermore, Aβ (25-35)-induced decreases in glutathione and increases in lipid peroxidation and cholinesterase activity in brain tissue were inhibited by RBO, and Aβ (25-35)-induced increases of phosphorylated mitogen-activated protein kinases (MAPKs) and inflammatory factors, and changes in the levels of apoptosis-related proteins were significantly inhibited by RBO. Furthermore, Aβ (25-35) suppressed the PI3K/Akt pathway and the phosphorylation of CREB, but increased phosphorylation of tau (p-tau) in mice brain; these effects were significantly inhibited by administration of RBO. These results suggest that RBO inhibits Aβ (25-35)-induced memory impairment by inducing anti-apoptotic and anti-inflammatory effects, promoting PI3K/Akt/CREB signaling, and thus, inhibiting p-tau formation.

• Computers and Concrete
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• v.18 no.3
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• pp.337-354
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• 2016

To study the influence on fracture properties of reinforced concrete wedge splitting test specimens by the addition of reinforcement, and the restriction of steel bars on crack propagation, 7 groups reinforced concrete specimens of different reinforcement position and 1 group plain concrete specimens with the same size factors were designed and constructed for the tests. Based on the double-K fracture criterion and tests, fracture toughness calculation model which was suitable for reinforced concrete wedge splitting tensile specimens has been obtained. The results show that: the value of initial craking load Pini and unstable fracture load Pun decreases gradually with the distance of reinforcement away from specimens's top. Compared with plain concrete specimens, addition of steel bar can reduce the value of initial fracture toughness KIini, but significantly increase the value of the critical effective crack length ac and unstable fracture toughness KIun. For tensional concrete member, the effect of anti-cracking by reinforcement was mainly acted after cracking, the best function of preventing fracture initiation was when the steel bar was placed in the middle of the crack, and when the reinforcement was across the crack and located away from crack tip, it plays the best role in inhibiting the extension of crack.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.12
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• pp.7439-7444
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• 2013

Aim: ATF3, a member of the ATF/CREB family of transcription factors, has been found to be selectively induced by calcineurin/NFAT inhibition and to enhance keratinocyte tumor formation, although the precise role of ATF3 in human skin cancer and possible mechanisms remain unknown. Methods: In this study, clinical analysis of 30 skin cancer patients and 30 normal donors revealed that ATF3 was accumulated in skin cancer tissues. Functional assays demonstrated that ATF3 significantly promoted skin cancer cell proliferation. Results: Mechanically, ATF3 activated Stat3 phosphorylation in skin cancer cell through regulation of p53 expression. Moreover, the promotion effect of ATF3 on skin cancer cell proliferation was dependent on the p53-Stat3 signaling cascade. Conclusion: Together, the results indicate that ATF3 might promote skin cancer cell proliferation and enhance skin keratinocyte tumor development through inhibiting p53 expression and then activating Stat3 phosphorylation.

• Journal of Microbiology and Biotechnology
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• v.25 no.12
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• pp.1997-2006
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• 2015

Ginsenoside Rg3 is a bioactive ginseng constituent that has been reported to have diverse pathological and physiological effects, including anti-inflammatory and anti-metastatic activities. Metastasis is one of the most important factors involved in patients with melanoma. However, the molecular mechanism underlying the anti-metastatic activities of Rg3 in malignant melanoma cancer has not been fully elucidated. In this study, we have evaluated that Rg3 effectively inhibits metastasis of B16F10 melanoma cancer cells. We found that Rg3 significantly suppresses the migration, invasion, wound healing, and colony-forming abilities of B16F10 cells in a dose-dependent manner. Mechanistically, we demonstrate that Rg3 suppresses B16F10 cell metastasis by inhibiting MMP-13 expression. These results indicate that Rg3 suppresses the metastasis of B16F10 mouse melanoma cancer cells via MMP-13 regulation. Importantly, MMP-13 downregulation may influence the migration and invasion capabilities of melanoma cells and has been correlated with melanoma progression. Therefore, Rg3 is a potential therapeutic candidate that could be used to treat patients with metastatic melanoma.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.1
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• pp.83-90
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• 2017

Advanced age is one of the risk factors for vascular diseases that are mainly caused by impaired nitric oxide (NO) production. It has been demonstrated that endothelial arginase constrains the activity of endothelial nitric oxide synthase (eNOS) and limits NO generation. Hence, arginase inhibition is suggested to be vasoprotective in aging. In this study, we examined the effects of intravenous injection of Piceatannol, an arginase inhibitor, on aged mice. Our results show that Piceatannol administration reduced the blood pressure in aged mice by inhibiting arginase activity, which was associated with NO production and reactive oxygen species generation. In addition, Piceatannol administration recovered $Ca^{2+}$/calmodulin-dependent protein kinase II phosphorylation, eNOS phosphorylation and eNOS dimer stability in the aged mice. The improved NO signaling was shown to be effective in attenuating the phenylephrine-dependent contractile response and in enhancing the acetylcholine-dependent vasorelaxation response in aortic rings from the aged mice. These data suggest Piceatannol as a potential treatment for vascular disease.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.18
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• pp.8053-8058
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• 2016

Metformin is known as a hypoglycaemic agent that regulates glucose homeostasis by inhibiting liver glucose production and increasing muscle glucose uptake. Colorectal cancer (CRC) is one of the most common cancers worldwide, with about a million new cases diagnosed each year. The risk factors for CRC include advanced age, smoking, black race, obesity, low fibre diet, insulin resistance, and the metabolic syndrome. We have searched Medline for the metabolic syndrome and its relation to CRC, and metformin as a potential treatment of colorectal cancer. Administration of metformin alone or in combination with chemotherapy has been shown to suppress CRC. The mechanism that explains how insulin resistance is associated with CRC is complex and not fully understood. In this review we have summarised studies which showed an association with the metabolic syndrome as well as studies which tackled metformin as a potential treatment of CRC. In addition, we have also provided a summary of how metformin at the cellular level can induce changes that suppress the activity of cancer cells.