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Luteolin induces apoptotic cell death via antioxidant activity in human colon cancer cells
Kang, Kyoung Ah,Piao, Mei Jing,Ryu, Yea Seong,Hyun, Yu Jae,Park, Jeong Eon,Shilnikova, Kristina,Zhen, Ao Xuan,Kang, Hee Kyoung,Koh, Young Sang,Jeong, Yong Joo,Hyun, Jin Won Spandidos Publications 2017 International journal of oncology Vol.51 No.4
<P>The present study determined whether luteolin induces HT-29 colon cancer cell death through an antioxidant effect such as the activation of antioxidant enzymes. Luteolin decreased cell viability in human colon cancer cells (HT-29), whereas it had no effect on normal colon cells (FHC). Luteolin induced apoptosis by activating the mitochondria-mediated caspase pathway in HT-29 cells. Luteolin caused loss of the mitochondrial membrane action potential, increased mitochondrial Ca2+ level, upregulated Bax, downregulated Bcl-2, induced the release of cytochrome c from mitochondria to the cytosol, and increased the levels of the active forms of caspase-9 and caspase-3. Luteolin-induced apoptosis was accompanied by the activation of intracellular and mitochondrial reactive oxygen species scavenging through the activation of antioxidant enzymes, such as superoxide dismutase and catalase in HT-29 cells. Luteolin increased the level of reduced glutathione (GSH) and the expression of GSH synthetase, which catalyzes the second step of GSH biosynthesis. The apoptotic effect of luteolin was mediated by the activation of the mitogen-activated protein kinase signaling pathway. The present results indicate that luteolin induces apoptosis by promoting antioxidant activity and activating MAPK signaling in human colon cancer cells.</P>
Susara Ruwan Kumara, Madduma Hewage,Piao, Mei Jing,Kang, Kyoung Ah,Ryu, Yea Seong,Park, Jeong Eon,Shilnikova, Kristina,Jo, Jin Oh,Mok, Young Sun,Shin, Jennifer H.,Park, Yeonsoo,Kim, Seong Bong,Yoo, Su NATIONAL HELLENIC RESEARCH FOUNDATION 2016 ONCOLOGY REPORTS Vol.36 No.4
<P>Colorectal cancer is a common type of tumor among both men and women worldwide. Conventional remedies such as chemotherapies pose the risk of side-effects, and in many cases cancer cells develop chemoresistance to these treatments. Non-thermal gas plasma (NTGP) was recently identified as a potential tool for cancer treatment. In this study, we investigated the potential use of NTGP to control SNUC5 human colon carcinoma cells. We hypothesized that NTGP would generate reactive oxygen species (ROS) in these cells, resulting in induction of endoplasmic reticulum (ER) stress. ROS generation, expression of ER stress-related proteins and mitochondrial calcium levels were analyzed. Our results confirmed that plasma-generated ROS induce apoptosis in SNUC5 cells. Furthermore, we found that plasma exposure resulted in mitochondrial calcium accumulation and expression of unfolded protein response (UPR) proteins such as glucose-related protein 78 (GRP78), protein kinase R (PKR)-like ER kinase (PERK), and inositol-requiring enzyme 1 (IRE1). Elevated expression of spliced X-box binding protein 1 (XBP1) and CCAAT/enhancer-binding protein homologous protein (CHOP) further confirmed that ROS generated by NTGP induces apoptosis through the ER stress signaling pathway.</P>
Park, Jeong Eon,Hyun, Yu Jae,Piao, Mei Jing,Kang, Kyoung Ah,Ryu, Yea Seong,Shilnikova, Kristina,Zhen, Ao Xuan,Ahn, Mee Jung,Ahn, Yong Seok,Koh, Young Sang,Kang, Hee Kyoung,Hyun, Jin Won Elsevier 2018 Journal of Functional Foods Vol.46 No.-
<P><B>Abstract</B></P> <P>This study investigated the protective effect of mackerel-derived fermented fish oil (FFO) against UVB radiation-induced oxidative stress in human HaCaT keratinocytes and mouse skin tissue. FFO treatment scavenged UVB-induced intracellular reactive oxygen species and attenuated oxidative modifications including lipid peroxidation, protein carbonylation, and DNA damage. FFO treatment reduced UVB-induced apoptosis by reducing DNA fragmentation, caspase activation, and proapoptotic protein expression. UVB radiation activated phospho-extracellular signal-regulated kinase, phospho-c-Jun N-terminal kinase, and phospho-p38, whereas their specific inhibitors with FFO treatment abrogated the cell viability and apoptosis increased by UVB irradiation. FFO was more cytoprotective than docosahexaenoic acid, the main component of fish oil, against UVB exposure. Furthermore, the cytoprotective effect of FFO was evident in both UVB-exposed HaCaT cell and mouse models. Overall, these results demonstrate that FFO protects the skin against UVB-induced oxidative stress through antioxidant effects. FFO has the potential for development as a functional food against UVB-induced skin damage.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Mackerel-derived fermented fish oil (FFO) scavenged UVB-induced intracellular reactive oxygen species. </LI> <LI> FFO treatment attenuated UVB-induced oxidative skin cellular modifications and apoptotic cell death. </LI> <LI> FFO may be developed as a functional food against UVB-induced skin damage. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>FFO prevented epidermal damage including oxidative cellular damage and apoptotic cell death by directly inhibiting UVB radiation or decreasing ROS level induced by UVB radiation.</P> <P>[DISPLAY OMISSION]</P>
( Susara Ruwan Kumara Madduma Hewage ),( Mei Jing Piao ),( Kyoung Ah Kang ),( Yea Seong Ryu ),( Pattage Madushan Dilhara Jayatissa Fernando ),( Min Chang Oh ),( Jeong Eon Park ),( Kristina Shilnikova 한국응용약물학회 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.4
Previously, we demonstrated that galangin (3,5,7-trihydroxyflavone) protects human keratinocytes against ultraviolet B (UVB)-induced oxidative damage. In this study, we investigated the effect of galangin on induction of antioxidant enzymes involved in synthesis of reduced glutathione (GSH), and investigated the associated upstream signaling cascades. By activating nuclear factor-erythroid 2-related factor (Nrf2), galangin treatment significantly increased expression of glutamate-cysteine ligase catalytic subunit (GCLC) and glutathione synthetase (GSS). This activation of Nrf2 depended on extracellular signal-regulated kinases (ERKs) and protein kinase B (AKT) signaling. Inhibition of GSH in galangin-treated cells attenuated the protective effect of galangin against the deleterious effects of UVB. Our results reveal that galangin protects human keratinocytes by activating ERK/AKTNrf2, leading to elevated expression of GSH-synthesizing enzymes.
( Susara Ruwan Kumara Madduma Hewage ),( Mei Jing Piao ),( Kyoung Ah Kang ),( Yea Seong Ryu ),( Xia Han ),( Min Chang Oh ),( Uhee Jung ),( In Gyu Kim ),( Jin Won Hyun ) 한국응용약물학회 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.3
Human skin cells undergo pathophysiological processes via generation of reactive oxygen species (ROS) upon excessive exposure to ultraviolet B (UVB) radiation. This study investigated the ability of hesperidin (C28H34O15) to prevent apoptosis due to oxidative stress generated through UVB-induced ROS. Hesperidin significantly scavenged ROS generated by UVB radiation, attenuated the oxidation of cellular macromolecules, established mitochondrial membrane polarization, and prevented the release of cytochrome c into the cytosol. Hesperidin downregulated expression of caspase-9, caspase-3, and Bcl-2-associated X protein, and upregulated expression of B-cell lymphoma 2. Hesperidin absorbed wavelengths of light within the UVB range. In summary, hesperidin shielded human keratinocytes from UVB radiation-induced damage and apoptosis via its antioxidant and UVB absorption properties.
( Pattage Madushan Dilhara Jayatissa Fernando ),( Mei Jing Piao ),( Kyoung Ah Kang ),( Yea Seong Ryu ),( Susara Ruwan Kumara Madduma Hewage ),( Sung Wook Chae ),( Jin Won Hyun ) 한국응용약물학회 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.1
This study was designed to investigate the cytoprotective effect of rosmarinic acid (RA) on ultraviolet B (UVB)-induced oxidative stress in HaCaT keratinocytes. RA exerted a significant cytoprotective effect by scavenging intracellular ROS induced by UVB. RA also attenuated UVB-induced oxidative macromolecular damage, including protein carbonyl content, DNA strand breaks, and the level of 8-isoprostane. Furthermore, RA increased the expression and activity of superoxide dismutase, catalase, heme oxygenase- 1, and their transcription factor Nrf2, which are decreased by UVB radiation. Collectively, these data indicate that RA can provide substantial cytoprotection against the adverse effects of UVB radiation by modulating cellular antioxidant systems, and has potential to be developed as a medical agent for ROS-induced skin diseases.
Reduced Autophagy in 5-Fluorouracil Resistant Colon Cancer Cells
( Cheng Wen Yao ),( Kyoung Ah Kang ),( Mei Jing Piao ),( Yea Seong Ryu ),( Pattage Madushan Dilhara Jayatissa Fernando ),( Min Chang Oh ),( Jeong Eon Park ),( Kristina Shilnikova ),( Soo-young Na ),( 한국응용약물학회 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.3
We investigated the role of autophagy in SNUC5/5-FUR, 5-fluorouracil (5-FU) resistant SNUC5 colon cancer cells. SNUC5/5- FUR cells exhibited low level of autophagy, as determined by light microscopy, confocal microscopy, and flow cytometry following acridine orange staining, and the decreased level of GFP-LC3 puncta. In addition, expression of critical autophagic proteins such as Atg5, Beclin-1 and LC3-II and autophagic flux was diminished in SNUC5/5-FUR cells. Whereas production of reactive oxygen species (ROS) was significantly elevated in SNUC5/5-FUR cells, treatment with the ROS inhibitor N-acetyl cysteine further reduced the level of autophagy. Taken together, these results indicate that decreased autophagy is linked to 5-FU resistance in SNUC5 colon cancer cells.
3,4-Dicaffeoylquinic acid protects human keratinocytes against environmental oxidative damage
Hyun, Yu Jae,Piao, Mei Jing,Kang, Kyoung Ah,Ryu, Yea Seong,Zhen, Ao Xuan,Cho, Suk Ju,Kang, Hee Kyoung,Koh, Young Sang,Ahn, Mee Jung,Kim, Tae Hoon,Hyun, Jin Won Elsevier 2019 Journal of Functional Foods Vol.52 No.-
<P><B>Abstract</B></P> <P>Skin is exposed to several harmful environmental effects including ultraviolet B (UVB) and air pollution, the most harmful component of which is particulate matter (PM). Damaging effects of UVB and PM include the generation of cellular reactive oxygen species (ROS), lipid peroxidation, protein carbonylation, DNA damage, and apoptosis. A compound with the potential to protect the skin against environmental oxidative damage is 3,4-dicaffeoylquinic acid (DQA), an antioxidant found in plant matter, including the coffee bean. In this study, we investigated the protective effects of DQA against UVB- and PM-induced oxidative cell damage in cultured human keratinocytes (HaCaT). We demonstrated that UVB, and PM with a diameter <2.5 µm (PM<SUB>2.5</SUB>), induced cellular damage via oxidative stress, and this was mitigated by the antioxidative action of DQA.</P> <P><B>Highlights</B></P> <P> <UL> <LI> DQA scavenged environmental UVB and PM<SUB>2.5</SUB>-induced intracellular ROS. </LI> <LI> DQA treatment attenuated environmental oxidative stressed-skin cellular modifications and apoptotic cell death. </LI> <LI> FFO may be developed as a functional food against environmental oxidative stress-induced skin damage. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>Exposure of UVB or PM<SUB>2.5</SUB> increased intracellular ROS and induced oxidative stress in HaCaT cells. DQA protects against UVB or PM<SUB>2.5</SUB>-indeced oxidative damage. In addition, it protects against UVB-induced apoptosis through inhibiting activation MAPKs.</P> <P>[DISPLAY OMISSION]</P>
Hewage, Susara Ruwan Kumara Madduma,Piao, Mei Jing,Kang, Kyoung Ah,Ryu, Yea Seong,Han, Xia,Oh, Min Chang,Jung, Uhee,Kim, In Gyu,Hyun, Jin Won The Korean Society of Applied Pharmacology 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.3
Human skin cells undergo pathophysiological processes via generation of reactive oxygen species (ROS) upon excessive exposure to ultraviolet B (UVB) radiation. This study investigated the ability of hesperidin ($C_{28}H_{34}O_{15}$) to prevent apoptosis due to oxidative stress generated through UVB-induced ROS. Hesperidin significantly scavenged ROS generated by UVB radiation, attenuated the oxidation of cellular macromolecules, established mitochondrial membrane polarization, and prevented the release of cytochrome c into the cytosol. Hesperidin downregulated expression of caspase-9, caspase-3, and Bcl-2-associated X protein, and upregulated expression of B-cell lymphoma 2. Hesperidin absorbed wavelengths of light within the UVB range. In summary, hesperidin shielded human keratinocytes from UVB radiation-induced damage and apoptosis via its antioxidant and UVB absorption properties.
Fernando, Pattage Madushan Dilhara Jayatissa,Piao, Mei Jing,Kang, Kyoung Ah,Ryu, Yea Seong,Hewage, Susara Ruwan Kumara Madduma,Chae, Sung Wook,Hyun, Jin Won The Korean Society of Applied Pharmacology 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.1
This study was designed to investigate the cytoprotective effect of rosmarinic acid (RA) on ultraviolet B (UVB)-induced oxidative stress in HaCaT keratinocytes. RA exerted a significant cytoprotective effect by scavenging intracellular ROS induced by UVB. RA also attenuated UVB-induced oxidative macromolecular damage, including protein carbonyl content, DNA strand breaks, and the level of 8-isoprostane. Furthermore, RA increased the expression and activity of superoxide dismutase, catalase, heme oxygenase-1, and their transcription factor Nrf2, which are decreased by UVB radiation. Collectively, these data indicate that RA can provide substantial cytoprotection against the adverse effects of UVB radiation by modulating cellular antioxidant systems, and has potential to be developed as a medical agent for ROS-induced skin diseases.