• Journal of the Korean Society of Food Science and Nutrition
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• v.41 no.2
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• pp.283-288
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• 2012

Triacsin C, an inhibitor of acyl-CoA synthetase, is known to have antiatherosclerotic and vasodilatory activities. The aims of this study were to evaluate the effects of triacsin C on endotoxin-induced (lipopolysaccharide, LPS) inflammation in 3T3-L1 adipocytes and also to evaluate its synergistic effect with triacsin C and resveratrol, a potent antiinflammatory agent. Exposure to LPS for 18 hr increased secretion of IL-6 into the culture medium and mRNA expression of IL-6, MCP-1, TLR and iNOS. Pretreatment of triacsin C for 2 hr suppressed IL-6 accumulation in the medium and the induction of IL-6 expression by LPS, which was more effective than resveratrol treatment. The synergistic effect of triacsin C and resveratrol was found to reduce the expression of iNOS by LPS. However, neither triacsin C nor resveratrol affected the LPS-induced expression of MCP-1, TLR or iNOS. These findings indicate that triacsin C may be a local regulator of inflammation in the adipocyte, although detailed mechanisms are needed to elucidate this through further research.

• The Korean Journal of Zoology
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• v.27 no.2
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• pp.73-84
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• 1984

In order to investigate the effect of neurotransmitter on myoblast differentiation in vitro, the effects of dopamine and epinephrine on myoblast fusion and on the intracellular cAMP level in cultured myoblasts were examined. Dopamine $(3\\times10^{-5}M)$ and epinephrine $(3\\times10^{-5}M)$, when added at 34 hr after cell plating, markedly inhibited myoblast fusion, and dopamine was more potent than epinephrine. Both dopamine and epinephrine had no effect on intracellular cAMP level. At the same time, exogeneous dbcAMP, $PGE_1$, and aspirin were used to examine whether cAMP is involved in myoblast differentiation. dbcAMP $(1\\times10^{-4}M)$ inhibited myoblast fusion, whereas $PGE_1 (3\\times10^{-6}M)$ had no inhibitory effect, rather enhancing myoblast fusion. Aspirin, an inhibitor of PG synthetase, was shown to inhibit myoblast fusion. Possible mechanism by which dopamine or epinephrine at a specific concentration used inhibits myoblast fusion is discussed.

• Korean Journal of Food Science and Technology
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• v.53 no.3
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• pp.304-312
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• 2021

The present study aimed to develop new physiologically active ingredients from Angelica gigas. The polysaccharides purified from A. gigas, AGE-2c-I, showed potent anti-complementary activity in a dose-dependent manner. C₃ activation products were identified through crossed immuno-electrophoresis using anti-human C₃ antibodies and the anti-complementary activity of AGE-2c-I under Ca⁺⁺-free conditions suggests that AGE-2c-I may induce complementary activation via both alternative and classical pathways. In addition, AGE-2c-I augmented the production of various cytokines, such as interleukin (IL)-6, IL-10, IL-12, and tumor necrosis factor-α, by peritoneal macrophages. Furthermore, intravenous (i.v.) administration of AGE-2c-I dose-dependently enhanced natural killer cell cytotoxicity against YAC-1 lymphoma. In experimental lung metastasis, prophylactic i.v. administration of AGE-2c-I inhibited lung metastasis by 58% at 100 ㎍/mouse. From the above results, we suggest that AGE-2c-I purified from A. gigas has potent immune system-stimulating activities, and is a potentially promising food ingredient beneficial to human health.

• The Korean Journal of Malacology
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• v.13 no.2
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• pp.131-141
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• 1997

전북 김제시 심포에서 1994년 1월부터 12월까지 월별로 채집된 백합 Meretrix lusoria의 생식세포형성과정 및 생식주기를 , 조직학적으로 조사한 결과는 다음과 같다. 백합은 자웅이체이고 난생을 하며, 생식소는 내장낭의 간중장선의 하부로부터 족부의 근육부근까지 분포하며, 성숙되면 팽대되지만 방란, 방정 후에는 위축된다. 생식소는 많은 난자형성여포들과 정자형셩여포들로 구성되어 있다. 여포에는 호산성 세포와 미분화간충직들이 들어 있는데, 이들은 초기 생식세포의 영양물질로 제공되고 있으며, 생식소가 발달함에 따라 점차 소실된다. 초기활성기의 난원세포는 직경 10$\mu\textrm{m}$ 내외이며, 초기 난모세포는 난병을 여포벽에 부착한 채 성장을 하여 70$\mu\textrm{m}$ 내외의 완숙란으로 된다. 정원세포가 성장을 하여 정보세포, 정세포를 거쳐 변태를 마친 정자는, 정자형성소낭의 중앙 내강에 정자속을 형성한다. 방란, 방정을 마친 생식소는, 일부 미방출된 생식세포가 퇴화 흡수되면서 비활성기를 지나 이듬해 수온상승과 더불어 새로운 발달을 시작한다. 생식주기는 연속적인 5단계로 구분할 수 있는데, 초기 활성기(1-3월), 후기 활성디 (2-5월), 완숙기(4-8월), 부분 방출기(6-9월), 퇴화 및 비활성기(9-2월)로 구분할 수 있다. 산란은 6월 (22$^{\circ}C$)부터 9월 ($25^{\circ}C$)까지 지속되지만, 산란성기는 7월(27$^{\circ}C$)-8월(28$^{\circ}C$)이다. 생식소지수는 1월에 0.58을 나타내며 5월에 4.60으로 최대값을 나타낸 후, 6월부터 점차 감소하기 시작하여 12월과 1월에는 1.0미만에 머무른다.

• The Korean Journal of Food And Nutrition
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• v.22 no.4
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• pp.639-643
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• 2009

In this study, the antineoplastic effects of chitosan hydrolysates were assessed. The chitosan hydrolysates showed no cytotoxicity in in vitro trials using the normal cell line, Vero E6(Africa green monkey kidney cells). The $IC_{50}$ value of the chitosan hydrolysates on Vero E6 was 1,107.95 ${\mu}g/m{\ell}$. The hydrolysates exhibited in vitro antineoplastic activity in five human tumor (lung carcinoma, bladder carcinoma, colon carcinoma, stomach carcinoma, breast carcinoma) cell lines. The $IC_{50}$ values of the hydrolysates on A549, J82, SNU-C4, SNU-1, and ZR75-1 cells were 421.06, 417.99, 445.54, 380.65 and 460.49 ${\mu}g/m{\ell}$, respectively.

• The korean journal of orthodontics
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• v.33 no.6 s.101
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• pp.453-463
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• 2003

Mammalian cell is critically dependent on a continuous supply of oxygen. Even brief periods of oxygen deprivation can result in profound cellular damage. The aim of this study was to examine the possible mechanism of apoptosis in response to hypoxia in MC3T3E1 osteoblasts. MC3T3El osteoblasts under hypoxic conditions ($2\%$ oxygen) resulted in apoptosis in a time-dependent manner, determined by DNA fragmentation assay and nuclear morphology, stained with fluorescent dye (Hoechst 33258) Pretreatment with Z-VAD-FMK, a pancaspase inhibitor, or Z-DEVD-CHO, a specific caspase-3 inhibitor, suppressed the DNA ladder in response to hypoxia in a concentration dependent manner. An increase in caspase-3-like protease (DEVDase) activity was observed during apoptosis, but no caspase-l activity (YVADase) was detected. To confirm what caspases were involved in apoptosis, western blot analysis was performed using an anticaspase-3 or 6 antibody. The 17-kDa protein, that corresponds to the active products of caspase-3 and the 20-kDa protein of the active protein of caspase-6 were generated in hypoxia-challenged lysates, in which the full length forms of caspase-3 and 6 were evident. With a time course similar to caspase-3 and 6 activation, hypoxic stress also caused the cleavage of Lamin A, typical of caspase-6 activity. In addition, the hypoxic stress elicited the release of cytochrome c into the cytosol during apoptosis. These findings suggested that the activation of caspases accompanied by a cytochrome c release in response to hypoxia was involved in apoptotic cell death in MC3T3E1 osteoblasts.

• The Korean Journal of Zoology
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• v.24 no.3
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• pp.133-144
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• 1981

The ultrastructures of the pigment cells in the Asiatic land salamander (Hynobius leechi) dorsal skin were obtained by means of electron microscope. The results were as follows; 1. The pigment cells of the epidermis consisted of the melanocytes in the germinal layer and of the melanophores distributing to the keratinocyte layer. The traits of these cells in the epidermis were as follows: A. The nuclei of the melanocytes were round or oval in shape and appeared as partly small or large infoldings of the nuclear envelope. B. Rough-surfaced endoplasmic reticulums and Golgi complexes were well developed in infranuclear cytoplasm. Many ribosomes were mainly distributed around the perinuclear portion. C. The melanosomes of the melanocytes were observed as a found or an oval shape and strong electron-dense or less electron-dense melanosomes were observed. D. The infoldings of the nuclear envelope in the melanophore were partly found deeper than those of the melanocyte. The cytoplasm of the melanophore filled with melanosomes caused organelles not to be observed in that. 2. The pigment cells in the dermis were composed of the xanthophores just beneath basement membrane and the melanophores in the connective tissue. The traits of these cells in the dermis were as follows: A. The xanthophores contained round or oval vesicles, and these vesicles were divided into 6 types (type I pterinosome, type II pterinosome, type III pterinosomes, type iv pterinosome, type V pterinosome, type VI pterinosome). B. Most of the nuclei of the melanophores in the dermis were elongate in shape, and a portion of the nuclear envelope was deep infolded. C. Becuase the cytoplasm was filled with the melanosomes of the same electron-density, organelles were not observed in the cytoplasm. D. Two processes of the melanophore in the dermis extended in parallel with a xanthophore and the cytoplasm in those processes were filled with the melanosomes.

• Journal of Chest Surgery
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• v.36 no.12
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• pp.887-893
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• 2003

External stimuli increases intracellular (IC) $Ca^{2+}$, which increases extracellular (EC) $K^{+}$. To verify $K^{+}$ effects on the vascular contraction, we performed an experiment using mouse aortic endothelial cell. Meterial and Method: We examined the mouse aortic contractility changes as we measured the IC $Ca^{2+}$ change and ionic current by using the voltage clamp technique under different conditions such as: increasing EC $K^{+}$, removing endothelial cell, giving L-NAME (N-nitro-L-arginine methyl ester) which suppress nitric oxide formation, Ouabain which control N $a^{+}$ - $K^{+}$ pump and N $i^{2+}$ which repress N $a^{+}$-C $a^{2+}$ exchanger Result: When we increased EC $K^{+}$ from 6 to 12 mM, there was no change in aortic contractility. Aorta contracted with more than 12 mM of EC $K^{+}$. Ace-tylcholine (ACh) induced relaxation was inhibited with EC $K^{+}$ from 6 to 12 mM, but was not found after de-endothelialization or L-NAME treatment. ATP or ACh increased IC $Ca^{2+}$ in cultured endothelium. After maximal increase of IC $Ca^{2+}$, increasing EC $K^{+}$ from 6 to 12 mM made IC $Ca^{2+}$ decrease and re-decreasing EC $K^{+}$ to 6 mM made IC $Ca^{2+}$ increase. Ouabain and N $i^{2+}$ masked the inhibitory effect of endothelium dependent relaxation by increased EC $K^{+}$. Conclusion: These data indicate that increase in EC $K^{+}$ relaxes vascular smooth muscle and reduces $Ca^{2+}$ in the endothelial cells which inhibit endothelium dependent relaxation. This inhibitory mechanism may be due to the activation of N $a^{+}$- $K^{+}$ pump and N $a^{+}$-C $a^{2+}$ exchanger. $a^{+}$-C $a^{2+}$ exchanger.r.

• The Journal of the Korea Contents Association
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• v.9 no.11
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• pp.247-253
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• 2009

We investigated the cell growth rate according to the change of temperature of the Thermo-rod used for the local hyperthermia therapy. For this study, we fabricated the Thermo-rods (TR) using Duplex Stainless Steels having magnetic properties as well as non magnetic properties. To evaluate cell growth rates up to 15 days, we conducted cell proliferation test using cell counting methods. For the tests, the CAPEs and Osteoblats were seeded on the 6-we11 plates with the induction heated thermo-rods 30 mins a day for 15 days with 2 days interval and without induction heated thermo-rods as control group respectively. We calculated cell growth rates, 6 hours after heating. From the results, in case of CAPEs and Osteobalsts seeded groups, the cell growth rates in all groups increased drastically for 6 days after seeding, but decreased irregularly after 6 days. In conclusion, the cell growth rates showed no significant difference among all groups and it indicated that there were no effects of temperate ($41^{\circ}C$) on cell growth rates.

• Toxicological Research
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• v.17 no.3
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• pp.215-223
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• 2001

Cadmium is an ubiquitous toxic metal and chronic exposure to cadmium results in the accumulation of cadmium in the liver and kidneys. In contrast, acute exposure leads to damage mainly in the liver. Apoptosis induced by cadmium has been shown in many tissues in vivo and in cultured cells in vitro. However, the molecular mechanism of cadmium-induced apoptosis is not clear in hepatocyte. To investigate the induction of apoptosis in the hepatocyte, we used mouse hepatoma cell line, Hepalclc7 cells, and analysed the molecules that involved in cadmium-induced apoptosis. Cadmium induced the genomic DNA fragmentation, PARP cleavage, and activation of caspase-3 like protease. Caspase-9 cysteine protease was activated in a time-dependent manner but caspase-8 cysteine protease was not significantly activated in cadmium-treated Hepalclc7 cells. Cadmium also induced mitochondrial dysfunction including cytochrome c release from mitochondria, change oj mitochondrial membrane potential tranition, and tranlocation of Bax Protein into mitochondria. These results strong1y indicated that the signal Pathway of apoptotic death in cadmium-treated Hepalclc7 cells is modulated by caspase cascade via mitochondria.