1.Galangin (3,5,7-Trihydroxyflavone) Shields Human Keratinocytes from Ultraviolet B-Induced Oxidative Stress.
Susara Ruwan Kumara MADDUMA HEWAGE ; Mei Jing PIAO ; Ki Cheon KIM ; Ji Won CHA ; Xia HAN ; Yung Hyun CHOI ; Sungwook CHAE ; Jin Won HYUN
Biomolecules & Therapeutics 2015;23(2):165-173
Most skin damage caused by ultraviolet B (UVB) radiation is owing to the generation of reactive oxygen species. Phytochemicals can act as antioxidants against UVB-induced oxidative stress. This study investigated the protective effects of the flavone galangin against UVB-induced oxidative damage in human keratinocytes. Galangin efficiently scavenged free radicals and reduced UVB-induced damage to cellular macromolecules, such as DNA, lipids, and proteins. Furthermore, galangin rescued cells undergoing apoptosis induced by UVB radiation via recovering mitochondrial polarization and down-regulating apoptotic proteins. These results showed that galangin protects human keratinocytes against UVB radiation-induced cellular damage and apoptosis via its antioxidant effects.
Antioxidants
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Apoptosis
;
DNA
;
Free Radicals
;
Humans
;
Keratinocytes*
;
Oxidative Stress*
;
Phytochemicals
;
Reactive Oxygen Species
;
Skin
2.A Benzylideneacetophenone Derivative Induces Apoptosis of Radiation-Resistant Human Breast Cancer Cells via Oxidative Stress.
Jeong Eon PARK ; Mei Jing PIAO ; Kyoung Ah KANG ; Kristina SHILNIKOVA ; Yu Jae HYUN ; Sei Kwan OH ; Yong Joo JEONG ; Sungwook CHAE ; Jin Won HYUN
Biomolecules & Therapeutics 2017;25(4):404-410
Benzylideneacetophenone derivative (1E)-1-(4-hydroxy-3-methoxyphenyl) hept-1-en-3-one (JC3) elicited cytotoxic effects on MDA-MB 231 human breast cancer cells-radiation resistant cells (MDA-MB 231-RR), in a dose-dependent manner, with an IC₅₀ value of 6 μM JC3. JC3-mediated apoptosis was confirmed by increase in sub-G1 cell population. JC3 disrupted the mitochondrial membrane potential, and reduced expression of anti-apoptotic B cell lymphoma-2 protein, whereas it increased expression of pro-apoptotic Bcl-2-associated X protein, leading to the cleavage of caspase-9, caspase-3 and poly (ADP-ribose) polymerase. In addition, JC3 activated mitogen-activated protein kinases, and specific inhibitors of these kinases abrogated the JC3-induced increase in apoptotic bodies. JC3 increased the level of intracellular reactive oxygen species and enhanced oxidative macromolecular damage via lipid peroxidation, protein carbonylation, and DNA strand breakage. Considering these findings, JC3 is an effective therapy against radiation-resistant human breast cancer cells.
Apoptosis*
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bcl-2-Associated X Protein
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Breast Neoplasms*
;
Breast*
;
Caspase 3
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Caspase 9
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Chalcone*
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DNA
;
Extracellular Vesicles
;
Humans*
;
Lipid Peroxidation
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Membrane Potential, Mitochondrial
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Mitogen-Activated Protein Kinases
;
Oxidative Stress*
;
Phosphotransferases
;
Protein Carbonylation
;
Reactive Oxygen Species
3.Protective Effect of Fisetin (3,7,3',4'-Tetrahydroxyflavone) against gamma-Irradiation-Induced Oxidative Stress and Cell Damage.
Mei Jing PIAO ; Ki Cheon KIM ; Sungwook CHAE ; Young Sam KEUM ; Hye Sun KIM ; Jin Won HYUN
Biomolecules & Therapeutics 2013;21(3):210-215
Ionizing radiation can induce cellular oxidative stress through the generation of reactive oxygen species, resulting in cell damage and cell death. The aim of this study was to determine whether the antioxidant effects of the flavonoid fisetin (3,7,3',4'-tetrahydroxyflavone) included the radioprotection of cells exposed to gamma-irradiation. Fisetin reduced the levels of intracellular reactive oxygen species generated by gamma-irradiation and thereby protected cells against gamma-irradiation-induced membrane lipid peroxidation, DNA damage, and protein carbonylation. In addition, fisetin maintained the viability of irradiated cells by partially inhibiting gamma-irradiation-induced apoptosis and restoring mitochondrial membrane potential. These effects suggest that the cellular protective effects of fisetin against gamma-irradiation are mainly due to its inhibition of reactive oxygen species generation.
Antioxidants
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Apoptosis
;
Cell Death
;
DNA Damage
;
Lipid Peroxidation
;
Membrane Potential, Mitochondrial
;
Membranes
;
Oxidative Stress*
;
Protein Carbonylation
;
Radiation, Ionizing
;
Reactive Oxygen Species
4.Extract of Curcuma zedoaria R. prevents atherosclerosis in apolipoprotein E-deficient mice
Ki Mo KIM ; Joo Young LEE ; Byeong Hwa JEON ; Khong Trong QUAN ; MinKyun NA ; Kung-Woo NAM ; Sungwook CHAE
Nutrition Research and Practice 2021;15(3):319-328
BACKGROUND/OBJECTIVES:
Curcuma zedoaria R. (Zingiberaceae) has been used to treat headache, fever, and hypertension-related symptoms in Asian countries, including Korea, China, and Japan. We investigated whether dietary intake of a C. zedoaria extract (CzE) affected atherosclerosis in vivo.MATERIALS/METHODS: Apolipoprotein E-deficient (ApoEM−/− ) mice (n = 32) were fed a normal diet (ND), a high-cholesterol diet (HCD), an HCD containing CzE (100 mg/kg/day), or an HCD containing simvastatin (10 mg/kg/day) for 12 weeks. The anti-atherosclerotic effects were evaluated by observing changes in fatty streak lesions, immunohistochemical analysis, ex vivo fluorescence imaging, lipid profiles, and western blot analysis.
RESULTS:
The CzE-fed group showed a 41.6% reduction of atherosclerosis. Furthermore, CzE significantly reduced the levels of serum triglyceride, high-density lipoprotein, the chemokine (C-X3-C-motif ) ligand 1, the adhesion molecules vascular cell adhesion molecule-1, intracellular adhesion molecule-1, and E-selectin; down-regulation of tumor necrosis factor-α, interleukin-6, high mobility group box-1, and cathepsin levels in the aortic sinuses and aortas of ApoE −/− mice were also observed.
CONCLUSIONS
The results suggest that the inclusion of a water extract of C. zedoaria in a HCD is closely correlated with reducing the risk of vascular inflammatory diseases in an ApoE mouse model.
5.Extract of Curcuma zedoaria R. prevents atherosclerosis in apolipoprotein E-deficient mice
Ki Mo KIM ; Joo Young LEE ; Byeong Hwa JEON ; Khong Trong QUAN ; MinKyun NA ; Kung-Woo NAM ; Sungwook CHAE
Nutrition Research and Practice 2021;15(3):319-328
BACKGROUND/OBJECTIVES:
Curcuma zedoaria R. (Zingiberaceae) has been used to treat headache, fever, and hypertension-related symptoms in Asian countries, including Korea, China, and Japan. We investigated whether dietary intake of a C. zedoaria extract (CzE) affected atherosclerosis in vivo.MATERIALS/METHODS: Apolipoprotein E-deficient (ApoEM−/− ) mice (n = 32) were fed a normal diet (ND), a high-cholesterol diet (HCD), an HCD containing CzE (100 mg/kg/day), or an HCD containing simvastatin (10 mg/kg/day) for 12 weeks. The anti-atherosclerotic effects were evaluated by observing changes in fatty streak lesions, immunohistochemical analysis, ex vivo fluorescence imaging, lipid profiles, and western blot analysis.
RESULTS:
The CzE-fed group showed a 41.6% reduction of atherosclerosis. Furthermore, CzE significantly reduced the levels of serum triglyceride, high-density lipoprotein, the chemokine (C-X3-C-motif ) ligand 1, the adhesion molecules vascular cell adhesion molecule-1, intracellular adhesion molecule-1, and E-selectin; down-regulation of tumor necrosis factor-α, interleukin-6, high mobility group box-1, and cathepsin levels in the aortic sinuses and aortas of ApoE −/− mice were also observed.
CONCLUSIONS
The results suggest that the inclusion of a water extract of C. zedoaria in a HCD is closely correlated with reducing the risk of vascular inflammatory diseases in an ApoE mouse model.
6.Isorhamnetin Protects Human Keratinocytes against Ultraviolet B-Induced Cell Damage.
Xia HAN ; Mei Jing PIAO ; Ki Cheon KIM ; Susara Ruwan Kumara MADDUMA HEWAGE ; Eun Sook YOO ; Young Sang KOH ; Hee Kyoung KANG ; Jennifer H SHIN ; Yeunsoo PARK ; Suk Jae YOO ; Sungwook CHAE ; Jin Won HYUN
Biomolecules & Therapeutics 2015;23(4):357-366
Isorhamnetin (3-methylquercetin) is a flavonoid derived from the fruits of certain medicinal plants. This study investigated the photoprotective properties of isorhamnetin against cell damage and apoptosis resulting from excessive ultraviolet (UV) B exposure in human HaCaT keratinocytes. Isorhamnetin eliminated UVB-induced intracellular reactive oxygen species (ROS) and attenuated the oxidative modification of DNA, lipids, and proteins in response to UVB radiation. Moreover, isorhamnetin repressed UVB-facilitated programmed cell death in the keratinocytes, as evidenced by a reduction in apoptotic body formation, and nuclear fragmentation. Additionally, isorhamnetin suppressed the ability of UVB light to trigger mitochondrial dysfunction. Taken together, these results indicate that isorhamnetin has the potential to protect human keratinocytes against UVB-induced cell damage and death.
Apoptosis
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Cell Death
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DNA
;
Fruit
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Humans
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Keratinocytes*
;
Plants, Medicinal
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Reactive Oxygen Species