• Proceedings of the Ginseng society Conference
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• 1988.08a
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• pp.47-54
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• 1988

Cholesterol a component of all eucaryotic plasma membranes. is essential for the growth and viability of cells in higher organisms. However. too much cholesterol can be lethal because of atherosclerosis resulting from the deposition of cholesterol ester plaques. It was attempted in this study to understand the preventive effect of ginseng saponin. one of the major components of the roots of Panax ginseng C.A. Meyer. against hypercholesterolemia induced by high cholesterol diet. $^{125}I-LDL$ was injected intravenously to rabbits and rats. which were fed a high cholesterol diet with and/or without ginseng saponin for 12 days. The disappearance of the radioactivity occurred faster in the test group than the control. The effect of saponin fraction from Panax ginseng C.A. Meyer and the purified ginsenosilks. $Rb_1,\;Rb_2,\;Re\;and\;Rg_1,$ on LDL receptor biosynthesis in high cholesterol fed rat has been investigated. Analysis of LDL receptors from various organs such as liver. kidney. adrenal cortex and testis showed that the population of LDL receptors of test group significantly higher than that of the control. It was also found that liver homogenate containing ginsenosides $(10^{-3}-10^{-4}\%)$ stimulated the biosynthesis of bile acid form cholesterol. From the above results. it seemed that ginsenosides lower the cholesterol level by stimulating cholesterol metabolism. which result in the suppression of the inhibitory action of cholesterol on LDL receptor biosynthesis.

• Journal of Life Science
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• v.27 no.9
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• pp.1020-1030
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• 2017

Epidemiology studies have reported a reduced incidence of colon cancer among populations that consume a large quantity of ${\omega}3-polyunsaturated$ fatty acids (${\omega}3-PUFAs$) of marine origin. Herein, we demonstrated a mechanism of anticancer action of ${\omega}3-PUFAs$, showing that they suppressed invasion and tumorigenicity in colon cancer cells. Docosahexaenoic acids (DHA) inhibited the cell growth of HT29 cells. This action likely involved apoptosis, given that the DHA treatment increased the cleaved form of PARP and sub G1 cells. Moreover, the invasiveness of HT29 cells was inhibited following DHA treatment, whereas arachidonic acid (AA) had no effect. The levels of Matrix-metalloproteinase-9 (MMP-9) and MMP-2 mRNA decreased after DHA pretreatment. DHA treatment inhibited MMP-9 and MMP-2 promoter activities and reduced VEGF promoter activity. DHA pretreatment also inhibited the activities of prostaglandin-2 (PGE2)-induced MMPs and the VEGF promoter. Cyclooxygenase-2 (COX-2) overexpression increased the activity of MMPs and that of the Vascular endotherial growth factor (VEGF) promoter in HT29 cells, and DHA inhibited NF-kB and COX-2 promoter reporter activities. As shown by in vivo experiments, when mouse colon cancer cells (MCA38) were implanted into Fat-1 and wild-type mice, both the tumoral size and volume were dramatically inhibited in Fat-1 transgenic mice. Furthermore, TUNEL-positive cells increased in tumors from Fat-1 mice compared with wild mice. In immunohistochemistry, the intensity of CD31 in Fat-1 tumors was weaker. These findings suggest that ${\omega}3-PUFAs$ may inhibit tumorigenicity and angiogenesis as well as cancer cell invasion by suppression of COX-2, MMPs and VEGF via the reduction of NF-kB in colon cancer.

• Journal of Nutrition and Health
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• v.23 no.3
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• pp.157-169
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• 1990

This study was designed to investigate the effect of supplementation of fish oil on serum apoprotein and platelet function in healthy young females. Eighteen female college students were divided into 3 groups. Each group fed a typical Korean diet supplemented with 15g, 12g, and 9g of fish oil respectively for 1-week. Blood samples were obtained 4 times, before supplementation, immediately after, 1-week after and 3-week after stopping supplementation. After 6-week break, the doses of fish oil were interchanged among 3 groups and the experiment was repeated to reduce interindividual variation. The concentration of apoprotein A, apoprotein B in the serum samples and the platelet adhesion, the platelet aggregation and bleeding time were determined immediately after supplementation of fish oil, 1-week after and 3-week after stopping supplementation and then the value compared with those of before supplementation period. The results obtained are summarized as follows: Serum apoprotein A levels decreased significantly(p<0.05), immediately after supplementation of fish oil in the 15g group. The serum apoprotein B levels did not show significant change. The platelet adhesion decreased significantly(p<0.05) 1-week after supplementation of fish oil in the 15g group. The platelet aggregation decreased significantly(p<0.01) immedeately after supplementation of fish oil in the 15g group.

• Journal of Nutrition and Health
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• v.48 no.6
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• pp.476-487
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• 2015

Purpose: This study was conducted to examine the concentration of nutrients in transitional breast milk from Korean lactating mothers and to evaluate daily intakes of their infants based on the Dietary Reference Intakes for Koreans 2010 (KDRIs 2010). Methods: Breast milk samples were collected at 5~15 days postpartum from 100 healthy lactating Korean mothers. Macro- and micro-nutrients, and immunoglobulin (Igs) concentrations in breast milk were analyzed. Results: The mean energy, protein, fat, and carbohydrate concentrations in breast milk were $59.99{\pm}8.01kcal/dL$, $1.47{\pm}0.27g/dL$, $2.88{\pm}0.89g/dL$, and $6.72{\pm}0.22g/dL$. The mean linoleic acid (LA), a-linolenic acid (ALA), arachidonic acid (AA), and docosahexaenoic acid (DHA) concentrations were $181.44{\pm}96.41mg/dL$, $28.15{\pm}8.89mg/dL$, $5.67{\pm}1.86mg/dL$, and $5.74{\pm}2.57mg/dL$. The mean vitamin A, vitamin D, vitamin E, vitamin $B_1$, vitamin $B_2$, vitamin $B_{12}$, and folate concentrations were $2.75{\pm}1.75{\mu}g/dL$, $2.31{\pm}1.12ng/dL$, $0.74{\pm}1.54mg/dL$, $3.02{\pm}1.84mg/dL$, $7.51{\pm}20.96{\mu}g/dL$, $61.78{\pm}26.78{\mu}g/dL$, $63.71{\pm}27.19ng/dL$, and $0.52{\pm}0.26{\mu}g/dL$. The mean concentrations of calcium, iron, potassium, sodium, zinc, and copper were $20.71{\pm}3.34mg/dL$, $0.59{\pm}0.86mg/dL$, $66.71{\pm}10.35mg/dL$, $27.72{\pm}10.16mg/dL$, $0.44{\pm}0.41mg/dL$, and $70.48{\pm}30.41{\mu}g/dL$. The mean IgA and total IgE concentrations were $61.85{\pm}31.97mg/dL$ and $235.00{\pm}93.00IU/dL$. The estimated daily intakes of infants for protein, vitamin D, vitamin E, vitamin $B_2$, vitamin $B_{12}$, iron, potassium, sodium, zinc, and copper were sufficient compared to KDRIs 2010 adjusted by transitory milk intakes. The estimated infants' intakes of energy, fat, carbohydrate, vitamin A, vitamin C, vitamin $B_1$, folate, and calcium did not meet KDRIs 2010 adjusted by transitory milk intakes. Conclusion: In general most estimated nutrient intakes of Korean breast-fed infants in transitory breast milk were sufficient, however some nutrient intakes were not sufficient based on KDRIs 2010. These results warrant conduct of future studies for investigation of important dietary factors associated with nutrients in breast milk to improve the quality of breast milk, which may contribute to understanding nutrition in early life and promoting growth and development of breast-fed infants.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.513-520
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• 1994

Background: The pathogenesis of silicosis has been focused on the interaction between alveolar macrophages and silica particle. Although fibrosis in silicosis has been studied extensively, the mechanism is still not fully understood. There is increasing evidence that monokines and arachidonic acid metabolites macrophage are involved in pathogenesis of silicosis. Recently, it was reported that prostaglandin E2 produced from macrophage counteracts the stimulatory effects of other monokines on fibroblast proliferation or collagen production. Until now, it was remained uncertain by which mechanism silica particle may activate alveolar macrophage to an enhanced release of prostaglandin E2. Methods: In order to investigate the relationship between the activity of alveolar macrophage and the production of $PGE_2$ from activated alveolar macrophage, the authors measured hydrogen peroxide and $PGE_2$ from alveolar macrophages activated by silica in vitro and from alveolar macrophages in the silicotic nodules from rat. Experimental silicosis was induced by intratracheal infusion of silica($SiO_2$) suspended in saline(50 mg/ml) in Sprague-Dawley rats. Results: produced by 1) The silicotic nodules with fibrosis were seen from the sections of rat lung at 60 days after intratracheal injection with 50 mg aqueous suspension of silica(Fig. 1). 2) In vitro, silica caused the dose dependent increase of hydrogen peroxide(p<0.05, Fig. 2A) and $PGE_2$(p>0.05, Fig. 2B) release from alveolar macrophages. Alveolar macrophages from rat with silicotic nodules released more hydrogen peroxide and $PGE_2$ than those of control group(p<0.05, Fig. 3). Conclusion: These results suggest that silica particle could activate macrophage directly and enhanced the release of $PGE_2$ and hydrogen peroxide from the alveolar macrophage.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.4
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• pp.1797-1802
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• 2014

Background: The prostaglandin-endoperoxide synthase 2 (PTGS2) and phospholipase A2 group IIA (PLA2G2A) genes encode enzymes that are involved in arachidonic acid and prostaglandin biosynthesis. Dysregulation of both genes is associated with inflammation and carcinogenesis, including esophageal squamous cell carcinoma (ESCC). We therefore hypothesized that there is an association between single nucleotide polymorphisms (SNPs) in these genes and susceptibility to ESCC. Methods: We performed a gene-wide tag SNP-based association study to examine the association of SNPs in PTGS2 and PLA2G2A with ESCC in 269 patients and 269 healthy controls from Taihangshan Mountain, Henan and Hebei Provinces, the rural area of China which has the highest incidence of esophageal cancer in the world. Thirteen tag SNPs in PLA2G2A and 4 functional SNPs in PTGS2 were selected and genotyped using a high-throughput Mass Array genotyping platform. Results: We found a modest increased risk of ESCC in subjects with the PTGS2 rs12042763 AA genotype (OR=1.23; 95% CI, 1.00-3.04) compared with genotype GG. For PLA2G2A, a decreased risk of ESCC was observed in subjects with the rs11677 CT (OR=0.51, 95%CI, 0.29-0.85) or TT genotype (OR=0.51, 95%CI, 0.17-0.96) or the T carriers (CT+TT) (OR=0.52, 95%CI, 0.31-0.85) when compared with the CC genotype. Also for PLA2G2A, rs2236771 C allele carriers were more frequent in the control group (P=0.02). Subjects with the GC (OR=0.55, 95%CI, 0.33-0.93) or CC genotype (OR=0.38, 95% CI, 0.16-0.94) or the C carriers (GC+CC) (OR=0.52, 95%CI, 0.32-0.85) showed a negative association with ESCC susceptibility. Conclusions: Our results suggest that PTGS2 and PLA2G2A gene polymorphisms may modify the risk of ESCC development.

• Journal of Life Science
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• v.21 no.7
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• pp.961-968
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• 2011

The formation of reactive lipid aldehydes, 4-hydroxynonenal (HNE) is shown to be derived from fatty acid hydroperoxides through the oxidative process. Among its known effects in cytotoxicity, HNE has been implicated in apoptotic cell death. To delineate its putative role as a potential mediator, we investigated the mechanism by which HNE induces apoptosis of endothelial cells (ECs). The anti-proliferative effects of HNE were tested through MTT assay after exposure to various concentrations ($5\sim15\;{\mu}M$) of HNE. We observed apoptotic bodies with propidium iodide staining, and measured the HNE induction of endothelial apoptosis by flow cytometry assay. We observed that cells exposed to HNE for 24 hr resulted in increased poly(ADP-ribose) polymerase cleavage and up-regulation of Bax. Data on the HNE action strongly indicated the involvement of reactive species, namely, intracellular ROS, nitrite, and peroxynitrite. To obtain evidence on the implication of ROS and peroxynitrite in HNE-induced apoptosis, a ROS scavenger, N-acetylcysteine (NAC), and a peroxynitrite scavenger, penicillamine, were tested. Results clearly indicate that the induction of apoptosis by HNE was effectively inhibited by NAC and penicillamine. Based on the present data, we conclude that the endothelial apoptosis induced by HNE involves both ROS generation and peroxynitrite activity. Our new data could lead to a redefinition of HNE action on apoptosis in ECs.

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.8
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• pp.979-984
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• 2006

Although iron is essential for many physiological processes, excess iron can lead to tissue damage by promoting the generation of reactive oxygen species (ROS). There is increasing evidence that ROS might play an important role in the pathogenesis of cardiovascular disease. However, the effects of iron excess on platelet function and the thrombotic response to vascular injury are not well understood. We examined the effects of iron excess-induced oxidative stress and the antioxidants on platelet aggregation. Oxidative stress was accessed by either free iron $(Fe^{+2})$ or hydrogen peroxide $(H_2O_2)$, as well as their combination on washed rabbit platelets (WPs) in vitro. When WPs were stimulated with either $Fe^{+2}$ alone or a subthreshold concentration of collagen, which gave an aggregatory curve with a little effect, and a dose dependent increase in platelet aggregation was observed by increasing concentrations of $Fe^{+2}$ with $H_2O_2$. This aggregation was associated with the iron-catalyzed formation of hydroxyl radicals from $H_2O_2$, and were inhibited by NAD/NADP (proton acceptor), catalase $(H_2O_2\;scavenger)$, tiron (iron chelator), mannitol (hydroxyl radical scavenger), and indomethacin (cyclooxygenase inhibitor), but not by NADH/NADPH (proton donor), superoxide mutase, and aspirin. However, NADH/NADPH, an essential cofactor for the antioxidant capacity by the supply of reducing potentials, showed the effect of an enhanced radical formation, suggesting a role for NADH/NADPH-dependent oxidase. These results suggest that iron $(Fe^{+2})$ can directly interact with washed rabbit platelets and this aggregation be mediated by OH formation as in the Fenton reaction, inhibited by radical scavengers.

• Proceedings of the KOR-BRONCHOESO Conference
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• 1978.06a
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• pp.4.1-4
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• 1978

The foreign bodies in the food and air passages are frequently observed in the field of otolaryngology, and the foreign bodies in the air passages have much significance in clinical practice because they may cause sudden death. A statistical study was done on 95 cases of foreign bodies in the food and air passages who had visited department of otolaryngology, Chung-Ang university from June, 1968 to April, 1978. The results were as follows; 1. The total cases of foreign bodies in the food and air passages was 95; 89 cases (93.7%) were in the food passage and the remaining (6.3%) were in the air passage. The ratio between the food passage and air passage was about 14. 8 to 1.0. 2. In distribution by sex, 64 cases (67.4%) were in male patients and the remaining 31 cases (32.6%) were in female patients. The ratio between male and female was 2.1 to 1.0. 3. The kinds of foreign bodies in the food in the order of their frequency, were coin, gogame stone and pebble. In the air passages, the peanut and bean were most frequently found. 4. In distribution by age, 64 cases (67.4%) of all foreign bodies were found in children under 5 year old, and coin was the most common kind of foreign body. Except for meat, almost all of foreign bodies were found in children under 10 year old. 5. There was chronologically no significant tendency in incidence; the incidence, however, had decreased during recent 2 years. 6. In the location of foreign bodies in the food passage, 70 cases (78.7%) were found at the first esophageal narrowing. Meat was more frequently found at second esophageal narrowing associated with cicatrical stenosis. Almost all of foreign bodies in the air passage was found in bronchi; 3 cases were in the right side of bronchi, and 2 cases were in the left side of bronchi and 1 case was in glottic region. 7. In duration of lodgement, 50 cases (52.6%) visited our hospital within 24 hours, and 3 cases after 30 days. 8. Under topical anesthesia, 83 cases (93.3%) of the foreign bodies in the food passage were removed by esophagoscopy, by 6 cases (6.7%) failed to be removed. All of the foreign bodies of the air passages (6 cases) were removed by bronchoscopy. Among them, 5 cases under 5 years old were removed by inferior bronchoscopy through tracheostomy site.

• The Korean Journal of Pharmacology
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• v.31 no.3
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• pp.299-311
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• 1995

Platelets resemble monoaminergic neurons in several respects, i.e. the uptake of 5-HT and its inhibition, the subcellular storage and release of 5-HT, and the metabolism of aromatic amines brought about by monoamine oxidase. And the 5-HT content of rabbit platelets is well known to be about 40 times higher than that of human platelets. Therefore, this study was carried out to investigate the influences of amitriptyline (AMT) and sertraline (SRT) on the aggregation, contents of signaling second messengers, and protein phosphorylations of rabbit platelets in response to thrombin, 0.25 unit/ml, comparing with those of chlorpromazine (CPZ). Thrombin-induced aggregation was inhibited by SRT $(IC50:4.37{\times}10^{-5}\;M)$, CPZ $(IC50:5.76{\times}10^{-5}\;M)$, and AMT $(IC50:1.15{\times}10^{-4}\;M)$, respectively, and the aggregation by A23187 $(1.0\;{\mu}M)$ or PMA (320 nM) was also inhibited by SRT, CPZ, and AMT. AMT, SRT, and CPZ had little affects on basal contents of platelet $TXB_2$ and $PGE_2$, but all of them inhibited the thrombin-induced increase of $TXB_2$. Thrombin did not change the platelet contents of cAMP and cGMP. CPZ, AMT, and SRT produced the slight decrease of basal cAMP content, and their effects were not affected by thrombin-treatment. But SRT and AMT moderately increased the basal cGMP content, and the cGMP content of thrombin-stimulated platelets was gradually increased by the pretreatment with SRT, AMT, and CPZ. Particularly, the SRT-dependent increase of the cGMP content was notable. Platelet $Ins(1,4,5)P_3$ content was rapidly increased up to a plateau within 10 sec after thrombin-stimulation, AMT, SRT, and CPZ increased the basal $Ins(1,4,5)P_3$ content, and the thrombin-dependent increase was enhanced by pretreatment with CPZ and AMT, but was blunted by SRT. Platelet $[Ca^{2+}]_i$, was rapidly increased up to a peak level within 20 sec after thrombin-stimulation. The increase of $[Ca^{2+}]_i$ was sisnificantly inhibited by AMT, SRT, and CPZ. Thrombin- or PMA-induced phosphorylations of platelet $41{\sim}43\;kDa$ and 20 kDa proteins were significantly inhibited by AMT, SRT, and CPZ. These results suggest that the antiplatelet activities of AMT and CPZ may be considerably attributed to the inhibition of protein kinase C activity, and the activity of SRT may be associated with the inhibitory effect on the thrombin-induced increase of $Ins(1,4,5)P_3$ and the increasing effect on the cGMP content of ptatelets. Therefore, it seems to be evident that AMT and SRT may produce their antidepressant activity, at least, partly through the inhibition of protein kinase C activity or the increase of resting $Ins(1,4,5)P_3$, content and in case of SRT, to a lesser extent, via the increase of cGMP in the brain.