• Journal of the Korean Chemical Society
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• v.62 no.5
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• pp.344-351
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• 2018

The IR spectra of gaseous phenanthrene, phenathrenols, phenanthrenyl radicals, and hydroxylphenanthrene radicals have been obtained using the BLYP/6-311++G(d,p) method. A comparison of these spectra shows that the measurements of IR spectra can be valuable to identify the reaction pathway(s) of the phenanthrene decomposition reaction by ${\cdot}OH$. We have found that the H atom abstraction reaction process can be easily identifiable from the $650-850cm^{-1}$ (CH out-of-plane bending) region and the ${\cdot}OH$ addition reaction process from the CH stretching and bending modes region of IR spectra. In addition, the calculated IR spectra of all five phenanthren-n-ols (n = 1, 2, 3, 4, 9) have also given in this work.

• Bulletin of the Korean Chemical Society
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• v.32 no.6
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• pp.1897-1901
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• 2011

This report shows the rates of solvolyses for phenyl methanesulfonyl chloride ($C_6H_5CH_2SO_2Cl$, I) in ethanol, methanol, and aqueous binary mixtures incorporating ethanol, methanol, acetone, 2,2,2-trifluroethanol (TFE) and 1,1,1,3,3,3-hexafluoro-2-propanol (HFIP) are reported. Three representative solvents, studies were made at several temperatures and activation parameters were determined. The thirty kinds of solvents gave a reasonably precise extended Grunwald-Winstein plot, coefficient (R) of 0.954. The sensitivity values (l = 0.61 and m = 0.34, l/m = 1.8) of phenyl methanesulfonyl chloride (I) were smaller than those obtained for benzenesulfonyl chloride ($C_6H_5SO_2Cl$, II; l = 1.01 and m = 0.61) and 2-propanesulfonyl chloride ($(CH_3)_2CHSO_2Cl$, III; l = 1.28 and m = 0.64). As with the two previously studied solvolyses, an $S_N2$ pathway with somewhat ionization reaction is proposed for the solvolyses of I. The activation parameters, ${\Delta}H^{\neq}$ and ${\Delta}S^{\neq}$, were determined and they are also in line with values expected for a bimolecular reaction mechanism. The kinetic solvent isotope effect of 2.34 in $CH_3OH/CH_3OD$ is in accord with a bimolecular mechanism, probably assisted by general-base catalysis.

• Animal Bioscience
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• v.35 no.7
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• pp.964-974
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• 2022

Objective: The highly pathogenic avian influenza virus (HPAIV) is a threat to the poultry industry and economy and remains a potential source of pandemic infection in humans. Antiviral genes are considered a potential factor for studies on HPAIV resistance. Therefore, in this study, we investigated gene expression related to the mitogen-activated protein kinase (MAPK) signaling pathway by comparing non-infected, HPAI-infected resistant, and susceptible Ri chicken lines. Methods: Resistant (Mx/A; BF2/B21) and susceptible Ri chickens (Mx/G; BF2/B13) were selected by genotyping the Mx and BF2 genes. Then, the tracheal tissues of non-infected and HPAIV H5N1 infected chickens were collected for RNA sequencing. Results: A gene set overlapping test between the analyzed differentially expressed genes (DEGs) and functionally categorized genes was performed, including biological processes of the gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathways. A total of 1,794 DEGs were observed between control and H5N1-infected resistant Ri chickens, 432 DEGs between control and infected susceptible Ri chickens, and 1,202 DEGs between infected susceptible and infected resistant Ri chickens. The expression levels of MAPK signaling pathway-related genes (including MyD88, NF-κB, AP-1, c-fos, Jun, JunD, MAX, c-Myc), cytokines (IL-1β, IL-6, IL-8), type I interferons (IFN-α, IFN-β), and IFN-stimulated genes (Mx1, CCL19, OASL, and PRK) were higher in H5N1-infected than in non-infected resistant Ri chickens. MyD88, Jun, JunD, MAX, cytokines, chemokines, IFNs, and IFN-stimulated expressed genes were higher in resistant-infected than in susceptible-infected Ri chickens. Conclusion: Resistant Ri chickens showed higher antiviral activity compared to susceptible Ri chickens, and H5N1-infected resistant Ri chickens had immune responses and antiviral activity (cytokines, chemokines, interferons, and IFN-stimulated genes), which may have been induced through the MAPK signaling pathway in response to H5N1 infection.

• Bulletin of the Korean Chemical Society
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• v.35 no.8
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• pp.2465-2470
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• 2014

The rate constants of solvolysis of phenyl N-phenyl phosphoramidochloridate (PhNHPO(Cl)OPh, Target Compound-TC1) have been determined by a conductivity method. The solvolysis rate constants of TC1 are well correlated with the extended Grunwald-Winstein equation, using the $N_T$ solvent nucleophilicity scale and YCl solvent ionizing scale, and sensitivity values of $0.85{\pm}0.14$ and $0.53{\pm}0.04$ for l and m, respectively. These l and m values were similar to those obtained previously for the complex chemical substances dimethyl thiophosphorochloridate; N,N,N',N'-tetramethyldiamidophosphorochloridate; 2-phenyl-2-ketoethyl tosylate; diphenyl thiophosphinyl chloride; and 9-fluorenyl chloroformate. As with the five previously studied solvolyses, an $S_N2$ pathway is proposed for the solvolyses of TC1. For four representative solvents, the rate constants were measured at several temperatures, and activation parameters (${\Delta}H^{\neq}$ and ${\Delta}S^{\neq}$) were estimated. These activation parameters are also in line with the values expected for an $S_N2$ reaction.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.3
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• pp.211-217
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• 2012

Recent studies have demonstrated that nitric oxide (NO) activates transient receptor potential vanilloid subtype 1 (TRPV1) via S-nitrosylation of the channel protein. NO also modulates various cellular functions via activation of the soluble guanylyl cyclase (sGC)/protein kinase G (PKG) pathway and the direct modification of proteins. Thus, in the present study, we investigated whether NO could indirectly modulate the activity of TRPV1 via a cGMP/PKG-dependent pathway in cultured rat dorsal root ganglion (DRG) neurons. NO donors, sodium nitroprusside (SNP) and S-nitro-N-acetylpenicillamine (SNAP), decreased capsaicin-evoked currents ($I_{cap}$). NO scavengers, hemoglobin and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (CPTIO), prevented the inhibitory effect of SNP on $I_{cap}$. Membrane-permeable cGMP analogs, 8-bromoguanosine 3', 5'-cyclic monophosphate (8bromo-cGMP) and 8-(4chlorophenylthio)-guanosine 3',5'-cyclic monophosphate (8-pCPT-cGMP), and the guanylyl cyclase stimulator YC-1 mimicked the effect of SNP on $I_{cap}$. The PKG inhibitor KT5823 prevented the inhibition of $I_{cap}$ by SNP. These results suggest that NO can downregulate the function of TRPV1 through activation of the cGMP/PKG pathway in peripheral sensory neurons.

• BMB Reports
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• v.57 no.2
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• pp.92-97
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• 2024

Elevated blood glucose is associated with an increased risk of atherosclerosis. Data from the current study showed that glucosamine (GlcN), a normal glucose metabolite of the hexosamine biosynthetic pathway (HBP), promoted lipid accumulation in RAW264.7 macrophage cells. Oleic acid- and lipopolysaccharide (LPS)-induced lipid accumulation was further enhanced by GlcN in RAW264.7 cells, although there was no a significant change in the rate of fatty acid uptake. GlcN increased acetyl CoA carboxylase (ACC), fatty acid synthase (FAS), scavenger receptor class A, liver X receptor, and sterol regulatory element-binding protein-1c (SREBP-1c) mRNA expression, and; conversely, suppressed ATP-binding cassette transporter A1 (ABCA-1) and ABCG-1 expression. Additionally, GlcN promoted O-GlcNAcylation of nuclear SREBP-1 but did not affect its DNA binding activity. GlcN stimulated phosphorylation of mammalian target of rapamycin (mTOR) and S6 kinase. Rapamycin, a mTOR-specific inhibitor, suppressed GlcN-induced lipid accumulation in RAW264.7 cells. The GlcN-mediated increase in ACC and FAS mRNA was suppressed, while the decrease in ABCA-1 and ABCG-1 by GlcN was not significantly altered by rapamycin. Together, our results highlight the importance of the mTOR signaling pathway in GlcN-induced macrophage lipid accumulation and further support a potential link between mTOR and HBP signaling in lipogenesis.

• Journal of the Korean Applied Science and Technology
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• v.37 no.3
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• pp.418-428
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• 2020

The aim of this study was to investigate the effect of resistance exercise(RE) on beta-amyloid(Aβ) metabolism, neuronal cell death, and cognitive function in the transgenic mice model of Alzheimer's disease(AD). Fourteen transgenic(tg) mice and fourteen non-transgenic(non-tg) mice were divided into four groups: (1)non-tg-control(NTC, n=7) (2)non-tg-RE(NTRE, n=7) (3)tg-control(TC, n=7), and (4)tg-RE(TRE, n=7). The groups with RE were performed to progressive RE on ladder equipment for 8 weeks. The groups with RE were performed to progressive RE on ladder equipment for 8 weeks. After then, the cognitive function was measured by using the water maze test, and Aβ metabolism-related proteins, neuronal cell death, and SIRT1/PGC-1α pathway were also measured. Here, we found escape latency and time were significantly increased in the TC compared to the NTC group, but it was significantly reduced in the TRE group, indicating RE may ameliorate cognitive dysfunction. Next, we found an increased in Aβ protein of TC compared to NTC, but it was significantly reduced in the TRE group following RE. In neuronal cell death, Bcl-2 was also significantly decreased and Bax was significantly increased in the TC compared to the NTC group, but RE can increase Bcl-2 and reduce Bax, which may elevate the ratio of Bcl-2/Bax. We further found a decrease in the level of ADAM10 and RARβ protein was significantly increased whereas increased in ROCK1 and BACE1 expression level was significantly reduced following RE in the TRE compared to the TC group. In addition, the level of SIRT1/PGC-1α proteins was decreased in the TC group compared to NTC group, but, these markers were significantly increased in the TRE group following RE. Therefore, our finding indicated that RE may ameliorate cognitive deficits by reducing Aβ protein and neuronal cell death via regulating SIRT1/PGC-1α, amyloidogenic pathway, and non-amyloidogenic pathway, which may play a role in an effective strategy for AD.

• Bulletin of the Korean Chemical Society
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• v.30 no.2
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• pp.383-388
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• 2009

Rates of solvolyses of diphenyl thiophosphorochloridate ($(PhO)_2$PSCl, 1) in ethanol, methanol, and aqueous binary mixtures incorporating ethanol, methanol, acetone and 2,2,2-trifluoroethanol (TFE) are reported. For four representative solvents, studies were made at several temperatures and activation parameters were determined. The 30 solvents gave a reasonably precise extended Grunwald-Winstein plot, correlation coefficient (R) of 0.989. The sensitivity values (l = 1.29 and m = 0.64) of diphenyl thiophosphorochloridate ($(PhO)_2$PSCl, 1) were similar to those obtained for diphenyl phosphorochloridate ($(PhO)_2$POCl, 2), diphenylphosphinyl chloride ($Ph_2$POCl, 3) and diphenylthiophosphinyl chloride ($Ph_2$PSCl, 4). As with the previously studied of 3~4 solvolyses, an $S_N$ pathway is proposed for the solvolyses of diphenyl thiophosphorochloridate (1). The activation parameters, ${\Delta}H^{\neq}\;(=11.6{\sim}13.9\;kcal{\cdot}mol^{-1})\;and\;{\Delta}S^{\neq}\; (=\;-32.1\;{\sim}\;-42.7\;cal{\cdot}mol^{-1}{\cdot}K^{-1})$, were determined, and they were in line with values expected for an $S_N$2 reaction. The large kinetic solvent isotope effects (KSIE, 2.44 in MeOH/MeOD and 3.46 in $H_2O/D_2$O) are also well explained by the proposed $S_N$2 mechanism.

• Bulletin of the Korean Chemical Society
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• v.29 no.10
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• pp.1927-1931
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• 2008

Rate of solvolysis of diphenylthiophosphinyl chloride in ethanol, methanol, and aqueous binary mixtures incorporating ethanol, methanol, acetone, 2,2,2-trifluoroethanol (TFE) or 1,1,1,3,3,3-hexafluoro-2-propanol (HFIP) are reported. Solvolyses were also carried out in TFE-ethanol mixtures. For five representative solvents, studies were made at several temperatures and activation parameters determined. The 29 solvents gave a reasonably precise extended Grunwald-Winstein equation plot, correlation coefficient (R) of 0.933, which improved to 0.983 when the four TFE-ethanol points were excluded. The sensitivities (l = 1.00 and m = 0.64) were similar to those obtained for dimethyl phosphorochloridate and phosphorochloridothionate and diphenylphosphinyl chloride (1). As with the four previously studied solvolyses, an $SN_2$ pathway is proposed for the solvolyses of diphenylthiophosphinyl chloride. The activation parameters, ${\Delta}H^{\neq}$ and ${\Delta}S^{\neq}$, were determined and they are also in line with values expected for an $S_N2$ reaction.

• Toxicological Research
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• v.24 no.2
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• pp.93-100
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• 2008

Targeting protein kinases has been active area in drug discovery. The c-Jun N-terminal kinases(JNKs) have also been target for development of novel therapy in various diseases, since the roles of JNK signaling in pathological conditions were revealed in studies using jnk-deficient mice. Small molecule inhibitors and peptide inhibitors are identified for therapeutic intervention of JNK signaling pathway. SP-600125, an anthrapyrazole small molecule inhibitor for JNK with high potency and selectivity has been widely used for dissecting JNK signaling pathway. CC-401 is the first JNK inhibitor that went into clinical trial for inflammation and leukemia. Inhibitor for mixed lineage kinase (MLK), CEP-1347 also negatively regulates JNK signaling, and tried for potential use in Parkinson's disease. Cell-permeable peptide inhibitor D-JNKI-1 is being developed for the treatment of hearing loss. The current status of these JNK inhibitors and safety issue is discussed in the minireview.