• The Journal of Dong Guk Oriental Medicine
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• v.7 no.1
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• pp.43-51
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• 1998

Renal tissues of ICR mouse were intraperitoneally injeced with Porpbyra yezoensis extract(PE) after Triton WR-1339(TX) injection were observed to investigate the cholesterol accumulation decreasing effect of PE. The renal tissues were obtained at hour 24, 48, and 72 after TX injection that were fixed in fromol-calcium solution and were cryocut. The tissue stained by sudan black B for lipid and perchloric acid-naphthoquinone method for cholesterol. The parietal layer of Bowman's capsule is swelled as cuboidal type at hour 48 after TX injection and the lipid blot and cholesterol particle were noticeably increased in glomerulus and these appeared in convoluted tubule, collecting tubule, and Helen's loop. In PE treated group, the lpid blot and cholesterol particle were considerably decreased in glomerulus than TX group. As results indicated that the accumulation of lipid including cholesterol caused by TX injection were mitigated in renal tissues by the antihypercholesterolemia effect of PE.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.3
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• pp.203-208
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• 2013

As the abnormal proliferation of vascular smooth muscle cells (VSMCs) plays a critical role in the development of atherosclerosis and vascular restenosis, a candidate drug with antiproliferative properties is needed. We investigated the antiproliferative action and underlying mechanism of a newly synthesized naphthoquinone derivative, 5,8-dimethoxy-2-nonylamino-naphthalene-1,4-dione (2-nonylamino-DMNQ), using VSMCs treated with platelet-derived growth factor (PDGF). 2-Nonylamino-DMNQ inhibited proliferation and cell number of VSMCs induced by PDGF, but not epidermal growth factor (EGF), in a concentration-dependent manner without any cytotoxicity. This derivative suppressed PDGF-induced $[^3H]$-thymidine incorporation, cell cycle progression from $G_0/G_1$ to S phase, and the phosphorylation of phosphor-retinoblastoma protein (pRb) as well as the expression of cyclin E/D, cyclin-dependent kinase (CDK) 2/4, and proliferating cell nuclear antigen (PCNA). Importantly, 2-nonylamino-DMNQ inhibited the phosphorylation of PDGF receptor${\beta}$(PDGF-$R{\beta}$) enhanced by PDGF at $Tyr^{579}$, $Tyr^{716}$, $Tyr^{751}$, and $Tyr^{1021}$ residues. Subsequently, 2-nonylamino-DMNQ inhibited PDGF-induced phosphorylation of STAT3, ERK1/2, Akt, and $PLC{\gamma}1$. Therefore, our results indicate that 2-nonylamino-DMNQ inhibits PDGF-induced VSMC proliferation by blocking PDGF-$R{\beta}$ autophosphorylation, and subsequently PDGF-$R{\beta}$-mediated downstream signaling pathways.

• Korean Journal of Weed Science
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• v.2 no.1
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• pp.41-46
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• 1982

Herbicidal effectivity on perennial paddy weeds such as Sagittaria pygmaea Miq. and Eleocharis kuroguwai Ohwi was evaluated. Herbicides used were butachlor [2-chloro-2, 6-dietyl-N(butoxymethyl)-acetanilide], benthiocarb [S-(4-chlorobenzy)-N, N-diethyl-thiocarbamate], molinate (S-ethyhexahyaro-l-Hazpine-carbothiate], SW-751, Chlormethoxynil (2.4-dichlorophenyl-3-methoxy-4-nitrophenyl-ether), CNP (2.4.6-trichlorophenyl-4-nitrophenylether),oxadiazon [2-tertbutyl-4-(2.4-dichloro-S-isopropoxyphenyl)-5-OXO-1.3.4-Oxadiazoline], dinuron [1-dimethyl-benthyl)-3-pheratrylurea], bentazon [3-isopropyl-IH-2.1.3-benzothiadiazine-(4)3H-one-2.2-dioxide], ACN (3-chloro-2-amino-l.4-naphthoquinone), MCPB [4-(2-methyl-4chlorophenoxy), butyric acid], 2.4-D (sodium 2.4-dichlorophenoxy acetic acid), MCP) sodium 2-methyl-4-chlorophenoxy acetic acid), SST-5, TH 63. Graszin D (Bentazon/2.4-D) and Graszin M (Bentazon/MCP) Herbicidal effectivity was divided into three types. Type I was the complete control both leaf and tuber, and SW-751 was belonged to this type. Type II was the partial control that exhibit complete control within certain period after herbicide application. After a certain period, however, the lateral bud have the germinability and grow normally, there after. Chloromethoxynil, CNP, ACN, and Oxadiazon were belonged to this group. Type III was no control at all. For E. kuroguwai, application of CNP, Chloromethoxnil, Oxadiazon and SW-751 gave good control in the early stage shile 2.4-D, MCP, bentazon and glaszin-D controlled well the intermediate stage application. Based on this results, E. kuroguwai can be controlled by herbicide application either in the early stage or in the intermediate stage.

• Proceedings of the Korean Biophysical Society Conference
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• 2003.06a
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• pp.80-80
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• 2003

${\beta}$-lapachone(${\beta}$-Lap), a natural o-naphthoquinone, presents in the bark of the Lapacho tree. ${\beta}$-Lap is cytotoxic against a variety of human cancer cells and it potentiates the anti-tumor effect of Taxol. In addition, ${\beta}$-Lap has been reported to radiosensitize cancer cells by inhibiting the repair of radiation-induced DNA damage.In the present study, we investigated the cytotoxicity of ${\beta}$-Lap against RKO human colorectal cancer cells as well as the combined effect of ${\beta}$-LaP and ionizing radiation. An incubation of RKO cells with 5 ${\mu}$M of ${\beta}$-Lap for 4 h killed almost 90％ of the clonogenic cells. An incubation of RKO cells with 5 ${\mu}$M of ${\beta}$-Lap for 4 h or longer also caused massive apoptosis. Unlike other cytotoxic agents, ${\beta}$-Lap did not increase the expression of p53 and p21 and it suppressed the NFkB expression. The expression of Caspase 9 and 3 was minimally altered by ${\beta}$-Lap. Radiation and ${\beta}$-Lap acted synergistically in inducing clonogenic cell death and apoptosis in RKO cells when ${\beta}$-Lap treatment was applied after but not before the radiation exposure of the cells. Interestingly, a 4 h treatment with 5 ${\mu}$M of ${\beta}$-Lap starting 5 h after irradiation was as effective as that starting immediately after irradiation. The mechanisms of ${\beta}$-Lap-induced cell killing is controversial but a recent hypothesis is that ${\beta}$-Lap is activated by NAD(P)H: quinone-onidoreductase (NQO1) in the cells followed by an elevation of cytosolic Ca$\^$2+/ level and activation of proteases leading to apoptosis. It has been reported that NQO1 level in cells is markedly up-regulated for longer than 10 h after irradiation. Indeed, using immunological staining of NQO1, we observed a significant elevation of NQO1 expression in RKO cells 5h after 2-4 Gy irradiation. Such a prolonged elevation of NQO1 level after irradiation may be the reasons why the ${\beta}$-Lap treatment applied S h after irradiation was as effective as that applied immediately after irradiation in killing the cells. In view of the fact that the repair of radiation-induced damage is usually completed within 1-2 h after irradiation, it is highly likely that the ${\beta}$-Lap treahment applied 5 h after irradiation could not inhibit the repair of radiation-induced damage. For in vivo study, RKO cells were injected S.C. into the hind-leg of Nu/Nu mice, and allowed to grow to 130 mm3 tumor. The mice were i.p. injected with ${\beta}$-lapachone or saline 2 h after irradiation of tumors with 10 Gy of X-rays. The radiation induced growth delay was increased by 2.4 $\mu\textrm{g}$/g of ${\beta}$-lapachone. Taken together, we may conclude that the synergistic interaction of radiation and ${\beta}$-Lap in killing cancer cells is not due to radiosensitization by ${\beta}$-Lap but to an enhancement of ${\beta}$-Lap cytotoxicity by radiation through an upregulation of NQO1. The fact that NQO1 is elevated in tumors and that radiation causes prolonged increase of the NQO1 expression may be exploited to preferentially kill tumor cells using ${\beta}$-Lap in combination with radiotherapy.