• 한국식품영양학회지
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• 제34권5호
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• pp.468-476
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• 2021

In recent years, there has been an increase in the morbidity of gastritis in Korea due to lifestyle factors mostly changes in eating habits and stress. Gastritis is more likely to progress to gastric cancer, and therefore it is important to prevent and manage gastritis through lifestyle adjustment and treatment at an early stage. In this study, cabbage, which was found to be effective in gastritis, was mixed and fermented with other crucifer plants such as kale and broccoli to evaluate the overall efficacy of fermented brassica puree on alcoholic acute gastritis. Based on our results, fermented brassica puree alleviated gastric injury induced by 150 mM HCl/60% ethanol. In addition, it was confirmed that PGE₂, a gastric mucosal protective factor, was increased, and other positive effects such as an increase of MUC1 and regulation of PKC were observed. The results of this study suggest that fermented brassica puree can relieve acute alcoholic gastritis by regulating PGE and the expression of MUC1, a gene related to mucus secretion, and activating PKC, which is related to mucosal cell activity.

• 한국임상수의학회지
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• 제26권1호
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• pp.8-16
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• 2009

항암제에 의해 흰쥐에서 다형핵 백혈구(polymorphonuclear leukocytes, PMN) 의 활성산소종(reactive oxygen species, ROS)과 산화질소(nitric oxide, NO)의 생성변화에 대해 연구하였다. 최근 자극유도인자에 의한 PMN의 호흡방출은 protein kinase C (PKC)의 활성, inositol phosphate transduction pathway의 활성, 그리고 intracellular [$Ca^{2+}$]와 관계가 있다고 밝혀졌으며, 본 연구에서 사용된 항암제(cyclophosphamide, cisplatin, tamoxifen, doxifluridine)중 일부는 화학치료제로써 비특이적으로 면역을 억제하는데 사용되고 있다. 암 치료 시 백혈구의 방어기능에 미치는 영향을 연구하기 위한 목적으로 in vitro에서 각 항암제를 처리한 PMN을 배양하여 ROS와 NO의 생성변화와 이차적 신호전달계인 phospholipase C(PLC), D(PLD), PKC, tyrosine phosphorylation kinase (TPK)와 phosphatidylinositol-3 kinase의 억제율을 측정하였다. PMN에 각각cyclophosphamide, cisplatin, tamoxifen, doxifluridine을 short term(${\leq}4hrs$) 처리시, formylmethionyl-leucy1-phenylalanine (FMLP) 자극에 의해 호흡방출의 증가가 나타났다. 반면, long term (8hrs) 처리 시, ROS의 생성은concentration-dependent 방법으로 감소되었다.

• 생명과학회지
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• 제20권5호
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• pp.655-661
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• 2010

흑색종세포주 SK-MEL-2에서 레티노이드에 의한 GD3합성효소(hST8Sia I)의 발현억제기작을 규명하게 위하여 hST8Sia I의 프로모터 활성을 조사해 본 결과 -1146에서 -646영역에서 레티노이드에 의한 활성억제를 나타내었다. 또한 부위특이적 변이와 ChIP분석은 -731에서 -722영역에 위치한 전사인자NF-kB 결합부위가 hST8Sia I의 레티노이드에 의한 활성억제에 중요하게 관여하고 있음을 나타내었다. 이러한 발현 억제는 PKC/ERK 신호전달경로를 통하여 일어난다는 것을 신호전달경로 저해제를 이용한 RT-PCR과 프로모터 활성조사에 의해 규명하였다.

• Biomolecules & Therapeutics
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• 제22권6호
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• pp.510-518
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• 2014

Chronic (>24 h) exposure of arsenite, an environmental toxicant, has shown the decreased nitric oxide (NO) production in endothelial cells (EC) by decreasing endothelial NO synthase (eNOS) expression and/or its phosphorylation at serine 1179 ($eNOS-Ser^{1179}$ in bovine sequence), which is associated with increased risk of vascular diseases. Here, we investigated the acute (<24 h) effect of arsenite on NO production using bovine aortic EC (BAEC). Arsenite acutely increased the phosphorylation of $eNOS-Thr^{497}$, but not of $eNOS-Ser^{116}$ or $eNOS-Ser^{1179}$, which was accompanied by decreased NO production. The level of eNOS expression was unaltered under this condition. Treatment with arsenite also induced reactive oxygen species (ROS) production, and pretreatment with a ROS scavenger N-acetyl-L-cysteine (NAC) completely reversed the observed effect of arsenite on $eNOS-Thr^{497}$ phosphorylation. Although protein kinase C (PKC) and protein phosphatase 1 (PP1) were reported to be involved in $eNOS-Thr^{497}$ phosphorylation, treatment with PKC inhibitor, Ro318425, and overexpression of various PKC isoforms did not affect the arsenite-stimulated $eNOS-Thr^{497}$ phosphorylation. In contrast, treatment with PP1 inhibitor, calyculin A, mimicked the observed effect of arsenite on $eNOS-Thr^{497}$ phosphorylation. Lastly, we found decreased cellular PP1 activity in arsenite-treated cells, which was reversed by NAC. Overall, our study demonstrates firstly that arsenite acutely decreases NO production at least in part by increasing $eNOS-Thr^{497}$ phosphorylation via ROS-PP1 signaling pathway, which provide the molecular mechanism underlying arsenite-induced increase in vascular disease.

• 대한핵의학회지
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• 제32권2호
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• pp.121-128
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• 1998

목적 : 생물학적 성질이 potassium과 유사하고 핵의학분야에서 널리 이용되고 있으며 쉽게 구할 수 있는 T1-201을 이용하여 $Na^+-K^+$ ATPase의 활성도를 측정할 수 있는지를 알아보고자, 배양한 백서 대동맥평활근세포와 사람의 제대동맥 평황근세포에서 $Na^+-K^+$ ATPase의 활성도를 측정하곤 기존의 Rb-86으로 측정한 방법과 비교하였다. 또한 T1-201로 측정한 활성도에 대한 포도당, 인슐린 및 PMA의 영향을 알아보고자 하였다. 대상 및 방법: Sprague-Dawley 백서의 흉부대동맥과 인체태반의 제대동맥에서 얻은 평활근세포를 배양하여 사용하였고. ouabain첨가로 억제되는 Rb-86과 T1-201의 섭취율을 $Na^+-K^+$ ATPase에 의한 섭취율로 계산하여 활성도로 간주하였다. 결과: 배양된 백서대동맥 평활근세포에서 $Na^+-K^+$ ATPase 활성도는 고포도당배양액(22 mM) 상태에서 생리적 농도의 저포도당배양액(5 mM) 상태에 비하여 평균 28%의 저하를 보였으며, 인슐린 100 nM을 첨가하였을 때는 50%의 증가를 보였다. PKC효소를 활성화시키는 PMA는 20%의 증가를 나타내었다. 인체제대동맥의 평활근세포에서도 유사한 변화를 보였다. T1-201로 측정한 $Na^+-K^+$ ATPase의 활성도치의 변화는 Rb-86을 이용한 측정에서도 동일하게 나타났다. 결론: T1-201을 이용하여 측정한 $Na^+-K^+$ ATPase 황성도는 Rb-86을 이용한 측정치와 유사하여, T1-201은 세포막 $Na^+-K^+$ ATPase 활성도의 측정에 사용할 수 있으리라 판단된다. 인슐린과 PKC효소 자극제는 $Na^+-K^+$ ATPase 활성도를 증가시키고, 고농도의 포도당은 활성도를 감소시키는 것으로 사료된다.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1998년도 Proceedings of UNESCO-internetwork Cooperative Regional Seminar and Workshop on Bioassay Guided Isolation of Bioactive Substances from Natural Products and Microbial Products
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• pp.156-157
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• 1998

Taurine is synthesized in the body or uptaken from dietary and is distributed in the various organs. It differs from other amino acids by virtue of the fact that a sulfonic acid group replaces the carboxyl group of what would be ${\beta}$-alanine. In order to function within the cell it must be transported into the cells by taurine transporter that is spanned 12 transmembrane domains. The human taurine transporter has long cytoplasmic carboxy and amino termini that may function as regulatory attachment sites for other proteins. Six potential protein kinase C(PKC) phosphorylation sites have been reported in human taurine transporter.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 1997년도 학술발표회
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• pp.28-28
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• 1997

Stimulation of $\alpha$$_1$-adrenergic receptor ($\alpha$$_1$-AR) by phenylephrine produced a decrease in intracellular N $a^{＋}$ activity ( $a_{Na}$ $^{i}$ ) in multicellular preparations of cardiac tissues. The role of protein kinase C (PKC) in $\alpha$$_1$-adrenergic regulation of $a_{Na}$ $^{i}$ was studied in single ventricular myocyte isolated from guinea pig hearts. $a_{Na}$ $^{i}$ and membrane potential were measured with N $a^{+}$ indicator, sodium-binding benzofuran isophthalate tetraacetoxy methyl ester (SBFI/AM) and microelectrodes respectively when ventricular myocyte was stimulated at 0.3 Hz.(omitted)d)

• 대한한의학회지
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• 제23권3호
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• pp.145-163
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• 2002

Objectives: The purpose of this investigation was to evaluate the effects of Woohwangcheongsim-won and to study the mechanism for neuronal death protection in hypoxia with Embryonic day 20 (E20) cortical cells of a rat (Sprague Dawley). Methods: E20 cortical cells were dissociated in neurobasal media and grown for 14 days in vitro (DIV). On 14 DIV, Woohwangcheongsim-won was added to the culture media for 24 hrs or 72 hrs. On 17 DIV, cells were given a hypoxic shock and further incubated in normoxia for another three days. On 20 DIV, Woohwangcheongsim-won's effects for neuronal death protection were evaluated by LDH assay, propidium iodide stain and phospho-H2AX immunostain and the mechanisms were studied by Bcl-2, Bak, Bax, caspase family, PKCα, ca1pain I. Results & Conclusions : 1. This study indicated that Woohwangcheongsim-won's effects for neuronal death protection in hypoxia were confirmed by LDH assay, propidium iodide stain and phospho-H2AX immunostain in culture method of Embryonic day 20(E20) cortical neuroblasts. 2. Woohwangcheongsim-won's mechanisms for neuronal death protection in hypoxia are to reduce the membrane damage fraction, to restrain DNA truncate, to restrain inflow of cytochrome c into cellularity caused by Bak diminution, to reduce the caspase cascade intiator caspase-8 and the effector caspase-3, to reduce the calpain I activity and to increase PKCand its activity in the membrane fraction. (J Korean Oriental Moo 2002;23(3):145～163)

• Journal of Medicine and Life Science
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• 제17권2호
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• pp.41-46
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• 2020

Metformin, a predominantly prescribed anti-diabetic drug for decades, has gained new insights for its anti-tumor activity in a variety of cancer cells. Our previous studies also showed the obvious pro-apoptotic activity of metformin and the underlying action mechanisms in hepatocellular carcinoma cells. Together with apoptosis, autophagy is a crucial intracellular process to determine the survival or death of cells under some stressful environments. The present study aimed to determine the role of autophagy in metformin-induced death of H4IIE hepatocellular carcinoma cells. Metformin blocked the formation of autophagosome and the expression of LC3A, generally described as a biomarker of autophagy. Inhibition of AMPK reversed the metformin-induced blockade of autophagy. Antioxidant (NAC) suppressed the metformin-induced cell death but not affected LC3A. The inhibition of protein kinase C totally restored the metformin-suppressed expression of LC3A. In summary, our present study suggests that autophagy is an anti-apoptotic player in metformin-induced apoptosis in H4IIE cells.

• Journal of Microbiology and Biotechnology
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• 제8권1호
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• pp.74-80
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• 1998

CS-2l lymphoma cells that preferentially metastasize to lymph nodes after s.c. inoculation into BALB/c mice were grown in vitro in the presence of CA- 12 stromal cells isolated from lymph nodes. In order to obtain fundamental data on the identification and characterization of the soluble factors produced by CA-12 stromal cells, the conditioned medium of CA-12 stromal cells that inhibited apoptosis of CS-21 cells was examined. Various analytical treatments revealed that the soluble factors in CA-12 conditioned medium are very sensitive to heat treatment and trypsinization. Moreover CA-12 conditioned medium has an affinity with heparin but not with Con-A. In addition to these, the activity of CA-12 conditioned medium was blocked by H-7, a PKC inhibitor, but the conditioned medium could not induce the differentiation of thymocytes. We concluded that CA-12 conditioned medium contains stromal cell-derived apoptosis-inhibitory molecules that play an important role in proliferation of CS-2l cells by suppressing cell apoptosis.