• Journal of the Korean Chemical Society
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• v.33 no.5
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• pp.551-557
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• 1989

7-Alkyl-1,3-dihydroxyphenazine-5,10-dioxides were synthesized by the reaction of 1,3,5-trihydroxybenzene with 6-alkylbenzofuroxans which had been obtained from aniline and n-alkyl alcohols bearing butyl, hexyl and octyl group. 1,3-Dihydroxyphenazine-5,10-dioxide was also prepared by the reaction of 1,3,5-trihydroxybenzene with benzofuroxan. The surface tension of aqueous solutions of these phenazine dioxide derivatives was determined by surface tensiometer and it was found out that the surface tension decreased with an increase of the number of carbon in the alkyl group. The antimicrobial activities of these phenazine dioxide derivatives were investigated in terms of minimum inhibitory concentration by the common twofold dilution technique. The derivative bearing butyl group showed the highest activity among these derivatives examined. It was observed that the antimicrobial activity of these alkyl substituted phenazine dioxide derivatives was stronger than that of the unsubstituted phenazine dioxide derivative.

• YAKHAK HOEJI
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• v.36 no.5
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• pp.440-448
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• 1992

7-Substituted 2,3-dihydroxyphenazine 5,10-dioxides were synthesized by the reaction of 1,2,4-trihydroxybenzene with 6-substituted benzofuroxan derivatives which had been obtained from aniline derivativies bearing methoxy, methyl, acetyl and nitro group at the para position. 2,3-Dihydroxyphenazine 5,10-dioxide was also prepared by the reaction of 1,2,4-trihydroxybenzene with benzofuroxan. The antimicrobial activities of these phenazine dioxide were investigated in terms of minimum inhibitory concentration by the common twofold dilution technique. It was observed that the antimicrobial activity of the phenazine dioxides bearing electron releasing substituents was stronger than that of those bearing electron withdrawing substitutents. From this result, it was concluded that the antimicrobial activity of phenazine dioxide derivatives has a direct relationship with the electronic effect of the substituents.

• Biomolecules & Therapeutics
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• v.32 no.4
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• pp.499-507
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• 2024

Specific sensitivity of the skin to ultraviolet B (UVB) rays is one of the mechanisms responsible for widespread skin damage. This study tested whether 1,3,5-trihydroxybenzene (THB), a compound abundant in marine products, might inhibit UVB radiationinduced NADPH oxidase 4 (NOX4) in both human HaCaT keratinocytes and mouse dorsal skin and explore its cytoprotective mechanism. The mechanism of action was determined using western blotting, immunocytochemistry, NADP⁺/NADPH assay, reactive oxygen species (ROS) detection, and cell viability assay. THB attenuated UVB-induced NOX4 expression both in vitro and in vivo, and suppressed UVB-induced ROS generation via NADP⁺ production, resulting in increased cell viability with decreased apoptosis. THB also reduced the expression of UVB-induced phosphorylated AMP-activated protein kinase (AMPK) and phosphorylated c-Jun N-terminal kinase (JNK). THB suppressed UVB-induced NOX4 expression and ROS generation by inhibiting AMPK and JNK signaling pathways, thereby inhibiting cellular damage. These results showed that THB could be developed as a UV protectant.

• Applied Biological Chemistry
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• v.45 no.3
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• pp.168-172
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• 2002

Antioxidative activities of solvent fractions obtained from Korean Rhus vernicifera, being used in food industry and as a traditional medicine, were examined by the methods of DPPH scavenging activity, inhibitory effect on autooxidation of linoleic acid, nitrite scavenging activity and the inhibitory effect on xanthine oxidase activity. Ethyl acetate fraction showed potent antioxidative activities. Three compounds were isolated from the ethyl acetate fraction by rotatory locular counter current chromatography (RLCCC), Sephadex LH-20 column chromatography and HPLC. The isolated compounds were 1,2,3-trihydroxybezene, methyl 3,4,5-trihydroxybenzoate and 3,4,5-trihydroxybenzoic acid determined by GC/MS and, $^1H$ and $^{13}C$ NMR. Among the isolated compounds, methyl 3,4,5-trihydroxybenzoate showed the strongest antioxidative activity than artificial antioxidants, BHA and BHT in various methods. However, these isolated compounds did not show cytotoxicity effects on the human cancer cell lines. Therefore, we may suggest that methyl 3,4,5-trihydroxybenzoate can be used as a food additive possessing the potent antioxidative activity.

• Biomolecules & Therapeutics
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• v.29 no.1
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• pp.90-97
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• 2021

Ultraviolet B (UVB) radiation causes DNA base modifications. One of these changes leads to the generation of 8-oxoguanine (8-oxoG) due to oxidative stress. In human skin, this modification may induce sunburn, inflammation, and aging and may ultimately result in cancer. We investigated whether phloroglucinol (1,3,5-trihydroxybenzene), by enhancing the expression and activity of 8-oxoG DNA glycosylase 1 (Ogg1), had an effect on the capacity of UVB-exposed human HaCaT keratinocytes to repair oxidative DNA damage. Here, the effects of phloroglucinol were investigated using a luciferase activity assay, reverse transcription-polymerase chain reactions, western blot analysis, and a chromatin immunoprecipitation assay. Phloroglucinol restored Ogg1 activity and decreased the formation of 8-oxoG in UVB-exposed cells. Moreover, phloroglucinol increased Ogg1 transcription and protein expression, counteracting the UVB-induced reduction in Ogg1 levels. Phloroglucinol also enhanced the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) as well as Nrf2 binding to an antioxidant response element located in the Ogg1 gene promoter. UVB exposure inhibited the phosphorylation of protein kinase B (PKB or Akt) and extracellular signal-regulated kinase (Erk), two major enzymes involved in cell protection against oxidative stress, regulating the activity of Nrf2. Akt and Erk phosphorylation was restored by phloroglucinol in the UVB-exposed keratinocytes. These results indicated that phloroglucinol attenuated UVB-induced 8-oxoG formation in keratinocytes via an Akt/Erk-dependent, Nrf2/Ogg1-mediated signaling pathway.