• Journal of Forest and Environmental Science
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• v.34 no.5
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• pp.376-381
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• 2018

For the control of oak wilt caused by Raffaelea quercus-mongolicae, an antifungal microorganism, Streptomyces blastmyceticus, was used as a potential agent. Culture suspension of S. blastmyceticus was injected into Quercus mongolicae in the research forest of Kangwon National University by $ChemJet^{(R)}$ trunk injection and Macro-infusion at root flare injection. $Alamo^{(R)}$ (a.i., propiconazole 14.5%), a fungicide currently used for the control of oak wilt in USA, was also treated by both methods to compare the efficacy. For preventive efficacy, culture suspension of the pathogen was inoculated at 1 month after injection of either agent. Tested trees were cut at 3 months after treatment, stained with 1% Fuchsin acid, and then non-conductive area (NCA) and re-isolation frequency (RIF) of oak wilt fungus were compared among treatments. While NCA was the highest as 47.3% in pathogen only treatment, it was the lowest as 16.0% in sterilized water treatment by Macro-infusion. NCAs of Alamo treatment by Macro-infusion and ChemJet injection were 25.3% and 32.1%, respectively. NCA of S.blastmyceticus treatment by ChemJet injection was 32.3%, similar with Alamo treatment's by ChemJet injection. All treatments by either injection method showed significantly lower NCA compared to the pathogen only treatment. These results indicate that S. blastmyceticus injection shows the preventive efficacy against oak wilt disease by suppressing the growth of pathogen injected. NCA of Macro-infusion injection of sterilized water was lower as 16.0%, compared to 21.3% of ChemJet injection. It means that Macro-infusion is more effective in translocation of sterilized water than ChemJet injection by even distribution. RIF from wood discs of treated trees showed high in pathogen only treatment, but relatively low in S. blastmyceticus treatment. RIF results were correlated with NCA results. From the above results, it was confirmed that S. blastmyceticus showed preventive efficacy against oak wilt disease by ChemJet trunk or Macro-infusion at root flare injection.

• Korean journal of applied entomology
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• v.18 no.1 s.38
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• pp.43-48
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• 1979

This study was conducted to detect lead which is exhausted with gas from running automobiles and is considered to accumulate in cropping lands. Soil samples were taken from uplands and paddy fields with different distance from highways. atonic absorption spectrophotometer was applied for analysis. Results obtained are summarized as follows: 1. In the areas of Seoul toll gate and Jookjeon, Gyeonggi province, soils of fields within $3\~5$ meters from highway appeared to contain $11\~110\;ppm$ of lead. On the other hand, soils outside of $3\~5$ meters showed only natural background level of lead. 2. The maximum concentration of lead in Hwoedeuk area (Choong-nam p개vince) was 16.3 ppm and those of Kimhae and Dongrae areas were about 12 ppm. Low concentration of $1\~4\;ppm$ was observed in the areas, south of Daejeon along the Honam and Namhae highways. 3. Lead seemed to accumulate in the soil surface within the range of 0 to 5 centimeters which anable to expect little translocation to deeper layer of the soil. 4. lost of arable lands locates at least 15 meters apart from highways so that lead concentrations were lower than expected. No damage could be speculated with the present concentration of lead analyzed. This does not deny the necessity to the long term dectect of the possible pollutant.

• Biomedical Science Letters
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• v.2 no.2
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• pp.175-185
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• 1996

The mitogen-activated protein(MAP) kinase signal transduction pathway represents an important mechanism by which mitogen, such as serum and PMA, regulate cell proliferation and differentiation. Target substrates of the MAP kinase are located within several compartments containing plasma membranes and nucleus. We now report that serum addition induces proliferation of the P388 murine leukemia cell, but PMA does not, while both serum and PMA treatment cause translocation of the MAP kinase, mainly p42$^{mapk}$ isoform, from cytosol into the nucleus, which was monitored by immunoblot analysis using polyclonal anti-ERK1 antibodies. We investigated whether the MAP kinase was capable of phosphorylating c-Jun protein and GST-fusion proteins, the P562$^{kk}$N-terminal peptides (1-77 or 1-123 domain) of the T cell tyrosine kinase, using the partially purified MAP kinase by SP-sephadex C-50, phenyl superose and Mono Q column chromatography. We found that the partially purified MAP kinase was able to phosphorylate c-Jun protein and the GST-fusion protein expressed using E.coli DH5$\alpha$ which is transformed with pGEX-3Xb plasmid vector carrying of p562$^{kk}$N-terminal peptide-encoding DNA. These results imply that tyrosine kinase receptor/Ras/Raf/MAP kinase pathway is a major mechanism for mitogen-induced cell proliferation in P388 murine leukemia cell and that the various MAP kinase isoforms may have their own target substrates located in distinct subcellular compartments.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.5
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• pp.986-992
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• 2009

Type I interferons (IFNs) are critical mediators of the innate immune system to defend viral infection. Interferon regulatory factor (IRF) and signal transducer and activator of transcription (STAT) play critical roles in type I IFN production in response to viral infection. Luteolin is natural polyphenolic compounds that have anti-inflammatory, cytoprotective and anti-carcinogenic effects. However, the mechanism of action and impact of luteolin on innate immunity is still unknown. In this study, we examined the effects of luteolin on the lipopolysacchride (LPS)-induced inflammatory responses. Luteolin inhibited Type I IFNs expression of mRNA and increased interleukin(IL)-10 expression of mRNA. Next, we examined the protective effects of IL-10 using IL-10 neutralizing antibody (IL-10NA). Blockade of IL-10 action didn't cause a significant reduction of Type I IFNs than LPS-induced luteolin pretreatment. Pretreatment of luteolin inhibited the level of IRF-1, and IRF-7 mRNA and the nuclear translocation of IRF-3. Also, luteolin reduced the activation of STAT - 1, 3. Theses results suggest that luteolin inhibits LPS-induced the production of Type I IFNS by both IRFs and STATs not IL-10 and may be a beneficial drug for the treatment of inflammatory disease.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05b
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• pp.88.2-98
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• 2002

A wide arry of naturally occurring substances particularly those present in dietary and medicinal plants, have been reported to possess substantial cancer chemopreventive properties. Certain phytochemicals retain strong antioxidative and anti-inflammatory properties which appear to contribute to their chemopreventive or chemoprotective activities. Inducible cyclooxygenase(COX-2) and nitric oxide synthase (iNOS) are important enzymes that mediate inflammatory processes. There is some evidence that expression of both COX-2 and iNOS is co-regulated by the eukaryotic transcription factor NF-$textsc{k}$B. Increased expression of COX-2 and/or iNOS has been associated with pathophysiology of certain types of human cancers as well as inflammatory diseases. Since inflammation is closely linked to tumor promotion, substances with potent anti-inflammatory activies are anticipated to exert chemopreventive effects on carcinogenesis, particularly in the promotion stage. An example is curcumin, a yellow pigment of turmeric (Curcuma longa L., Zingiberaceae), that strongly occurring diaryl heptanoids structurally related to curcumin have substantial anti-tumor promotional activities in two-stage mouse skin carcinogenesis. Thus, yakuchinone A [1-(4'-hydroxy-3'-methoxyphenyl)-7-phenyl-3heptanone] and yakuchinone B [1-(4'-hydroxy-3'methoxyphenyl)-7-phenylhept-1-en-3-one] present in Alpinia oxyphylla Miquel (Zingiberacease) attenuate phorbol ester-induced inflammation and papilloma formation in female ICR mice. These diarylheptanoids also suppressed phorbol ester-induced activation of epdermal ornithine decarboxylase and its mRNA expression when applied onto shaven backs of mice. Yakuchinone A and B as well as curcumin inhibited phorbol ester-induced expression of COX-2 and iNOS and their mRNA in mouse skin via inactivation of NF-$textsc{k}$B. Capsaicin, a major pungent ingredient of red pepper also attenuated phorbol ester-induced NF-$textsc{k}$B activation. Similar suppression of COX-2 and iNOS and down-regulation of NF-$textsc{k}$B activation for its DNA binding were observed with the ginsenosied Rg3 and the ethanol extract of Artemisia asiatica. We have also found that certain anti-inflammatory phytochemicals exert inhibitory effects on phorbol ester-induced COX-2 expression and NF-$textsc{k}$B activation in immortalized human breast epithelial (MCF-10A) cells in culture. One of the plausible mechanisms undelying inhibition by aforementioned phytochemicals of phorbol ester-induced NF-$textsc{k}$B activation involves interference with degragation of the inhibitory unit, I$textsc{k}$Ba, which blocks subsequent nuclear translocation of the functionally active p65 subunit of NF-$textsc{k}$B. the activation of epidermal NF-$textsc{k}$B by phorbol ester and subsequent induction of COX-2 hence appear to play an important role in intracellular signaling pathwasy leading to tumor promotion and targeted inhibition of NF-$textsc{k}$B may provide a new promising cancer chemopreventive strategy.

• Biomolecules & Therapeutics
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• v.24 no.5
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• pp.543-551
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• 2016

This study was designed to evaluate the pharmacological effects of Vaccinium bracteatum Thunb. methanol extract (VBME) on microglial activation and to identify the underlying mechanisms of action of these effects. The anti-inflammatory properties of VBME were studied using lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. We measured the production of nitric oxide (NO), inducible NO synthase (iNOS), cyclooxygenase (COX)-2, prostaglandin $E_2$ ($PGE_2$), tumor necrosis factor-alpha (TNF-${\alpha}$), interleukin-1 beta (IL-$1{\beta}$), and interleukin-6 (IL-6) as inflammatory parameters. We also examined the effect of VBME on intracellular reactive oxygen species (ROS) production and the activity of nuclear factor-kappa B p65 (NF-${\kappa}B$ p65). VBME significantly inhibited LPS-induced production of NO and $PGE_2$ and LPS-mediated upregulation of iNOS and COX-2 expression in a dose-dependent manner; importantly, VBME was not cytotoxic. VBME also significantly reduced the generation of the pro-inflammatory cytokines TNF-${\alpha}$, IL-$1{\beta}$, and IL-6. In addition, VBME significantly dampened intracellular ROS production and suppressed NF-${\kappa}B$ p65 translocation by blocking $I{\kappa}B-{\alpha}$ phosphorylation and degradation in LPS-stimulated BV2 cells. Our findings indicate that VBME inhibits the production of inflammatory mediators in BV-2 microglial cells by suppressing NF-${\kappa}B$ signaling. Thus, VBME may be useful in the treatment of neurodegenerative diseases due to its ability to inhibit inflammatory mediator production in activated BV-2 microglial cells.

• Biomolecules & Therapeutics
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• v.25 no.4
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• pp.417-426
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• 2017

4-O-methylhonokiol, a neolignan compound from Magnolia Officinalis, has been reported to have various biological activities including hair growth promoting effect. However, although transforming growth factor-${\beta}$ (TGF-${\beta}$) signal pathway has an essential role in the regression induction of hair growth, the effect of 4-O-methylhonokiol on the TGF-${\beta}$ signal pathway has not yet been elucidated. We thus examined the effect of 4-O-methylhonokiol on TGF-${\beta}$-induced canonical and noncanonical pathways in HaCaT human keratinocytes. When HaCaT cells were pretreated with 4-O-methylhonokiol, TGF-${\beta}1$-induced G1/G0 phase arrest and TGF-${\beta}1$-induced p21 expression were decreased. Moreover, 4-O-methylhonokiol inhibited nuclear translocation of Smad2/3, Smad4 and Sp1 in TGF-${\beta}1$-induced canonical pathway. We observed that ERK phosphorylation by TGF-${\beta}1$ was significantly attenuated by treatment with 4-O-methylhonokiol. 4-O-methylhonokiol inhibited TGF-${\beta}1$-induced reactive oxygen species (ROS) production and reduced the increase of NADPH oxidase 4 (NOX4) mRNA level in TGF-${\beta}1$-induced noncanonical pathway. These results indicate that 4-O-methylhonokiol could inhibit TGF-${\beta}1$-induced cell cycle arrest through inhibition of canonical and noncanonical pathways in human keratinocyte HaCaT cell and that 4-O-methylhonokiol might have protective action on TGF-${\beta}1$-induced cell cycle arrest.

• Journal of Life Science
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• v.20 no.9
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• pp.1332-1338
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• 2010

To elucidate the mechanism underlying the regulation of hST8Sia I gene expression in FenR-induced SH-SY5Y cells, we characterized the promoter region of the hST8Sia I gene. Functional analysis of the 5'-flanking region of the hST8Sia I gene showed that the -1146 to -646 region functions as the FenR-inducible promoter of hST8Sia I in SH-SY5Y cells. Site-directed mutagenesis indicated that the NF-&B binding site at -731 to -722 was crucial for the FenR-induced expression of hST8Sia I in SH-SY5Y cells. To investigate which signal transduction pathway was involved in FenR-stimulated induction of hST8Sia I in SH-SY5Y cells, we performed Western blot analysis using phospho-specific antibodies in order to measure their degree of regulatory phosphorylation. Phosphorylations of AKT and RelA (p65) subunit of NF-${\kappa}B$ were significantly elevated in cytosolic and nuclear fractions of FenR-stimulated SH-SY5Y cells, respectively, than in control or DMSO-treated SH-SY5Y cells. These results suggest that FenR induce transcriptional up-regulation of hST8Sia I gene expression through translocation of RelA (p65) subunit of NF-${\kappa}B$ to nucleus by AKT signal pathway in SH-SY5Y cells.

• Journal of Life Science
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• v.28 no.1
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• pp.43-49
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• 2018

Chrysoeriol is a widespread flavone, and it is usually found in alfalfa, which has been used as a traditional medicine to treat dyspepsia, asthma, and urinary system disorders. Recently, analysis has been conducted on the anti-inflammatory activity of chrysoeriol, but information on its antioxidative capacity is limited. In this study, the antioxidative potential of chrysoeriol against oxidative damage and its molecular mechanisms were evaluated by analysis of the cell viability, reactive oxygen species (ROS) formation, and Western blots in the RAW 264.7 cell line. Chrysoeriol significantly scavenged lipopolysaccharide (LPS)-induced intracellular ROS formation in a dose-dependent manner, without any cytotoxicity. Heme oxygenase-1 (HO-1), a phase II enzyme that exerts antioxidative activity, was also potently induced by chrysoeriol treatment, which corresponded to the translocation of nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) into the nucleus. Moreover, mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K) were analyzed due to their important role in maintaining cellular redox homeostasis against oxidative stress. As a result, chrysoeriol-induced HO-1 upregulation was mediated by extracellular signal - regulated kinase (ERK), c-Jun $NH_2$-terminal kinase (JNK), and p38 phosphorylation. To identify the antioxidative potential exerted by HO-1, tert-butyl hydroperoxide (t-BHP)-induced oxidative damage was applied and mitigated by chrysoeriol treatment, which was confirmed by the HO-1 selective inhibitor and inducer, respectively. Consequently, chrysoeriol strongly strengthened the HO-1-mediated antioxidative potential through the regulation of the Nrf2/MAPK signaling pathways.

• Molecules and Cells
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• v.37 no.12
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• pp.899-906
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• 2014

Prostaglandin $E_2$ ($PGE_2$) promotes tumor-persistent inflammation, frequently resulting in cancer. Curcumin is a diphenolic turmeric that inhibits carcinogenesis and induces apoptosis. $PGE_2$ inhibits curcumin-induced apoptosis; however, the underlying inhibitory mechanisms in colon cancer cells remain unknown. The aim of the present study is to investigate the survival role of $PGE_2$ and whether addition of exogenous $PGE_2$ affects curcumininduced cell death. HCT-15 cells were treated with curcumin and $PGE_2$, and protein expression levels were investigated via Western blot. Reactive oxygen species (ROS) generation, lipid peroxidation, and intracellular glutathione (GSH) levels were confirmed using specific dyes. The nuclear factor-kappa B ($NF-{\kappa}B$) DNA-binding was measured by electrophoretic mobility shift assay (EMSA). $PGE_2$ inhibited curcumin-induced apoptosis by suppressing oxidative stress and degradation of PARP and lamin B. However, exposure of cells to the EP2 receptor antagonist, AH6809, and the PKA inhibitor, H89, before treatment with $PGE_2$ or curcumin abolished the protective effect of $PGE_2$ and enhanced curcumin-induced cell death. $PGE_2$ activates PKA, which is required for cAMP-mediated transcriptional activation of CREB. $PGE_2$ also activated the Ras/Raf/Erk pathway, and pretreatment with PD98059 abolished the protective effect of $PGE_2$. Furthermore, curcumin treatment greatly reduced phosphorylation of CREB, followed by a concomitant reduction of $NF-{\kappa}B$ (p50 and p65) subunit activation. $PGE_2$ markedly activated nuclear translocation of $NF-{\kappa}B$. EMSA confirmed the DNA-binding activities of $NF-{\kappa}B$ subunits. These results suggest that inhibition of curcumin-induced apoptosis by $PGE_2$ through activation of PKA, Ras, and $NF-{\kappa}B$ signaling pathways may provide a molecular basis for the reversal of curcumin-induced colon carcinoma cell death.