The Experts below are selected from a list of 327 Experts worldwide ranked by ideXlab platform
Jin Won Hyun - One of the best experts on this subject based on the ideXlab platform.
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the cytoprotective effect of Butin against oxidative stress is mediated by the up regulation of manganese superoxide dismutase expression through a pi3k akt nrf2 dependent pathway
Journal of Cellular Biochemistry, 2012Co-Authors: Rui Zhang, Sungwook Chae, Jun Hwa Lee, Jin Won HyunAbstract:Butin (7,3′,4′-trihydroxydihydroflavone), a flavonoid with antioxidant activity, was recently reported to protect cells against H2O2-induced apoptosis, oxidative DNA damage and oxidative mitochondrial dysfunction. The objective of the present study was to elucidate the mechanism by which Butin protects mitochondria. The antioxidant function of manganese superoxide dismutase (Mn SOD) is important in preventing oxidative stress. While exposure to H2O2 reduced the expression of Mn SOD in Chinese hamster lung fibroblast (V79-4), the addition of Butin restored Mn SOD expression at both the mRNA and protein levels, resulting in increased Mn SOD activity. The transcription factor NF-E2-related factor 2 (Nrf2) regulates Mn SOD gene expression by binding to the antioxidant responsive element (ARE). Butin enhanced the nuclear translocation and ARE-binding activity of Nrf2, which was decreased by H2O2. The siRNA-mediated knockdown of Nrf2 attenuated Butin-induced Mn SOD expression and activity. Further, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB, Akt) contributed to the ARE-driven Mn SOD expression. Butin activated PI3K/Akt and exposure to either LY294002 (a PI3K inhibitor), Akt inhibitor IV (an Akt-specific inhibitor), or Akt siRNA suppressed the Butin-induced activation of Nrf2, resulting in decreased Mn SOD expression and activity. Finally, the cytoprotective effect of Butin against H2O2-induced cell damage was suppressed by the siRNA-mediated knockdown of Mn SOD. These studies demonstrate that Butin attenuates oxidative stress by activating Nrf2-mediated Mn SOD induction via the PI3K/Akt signaling pathway. J. Cell. Biochem. 113: 1987–1997, 2012. © 2012 Wiley Periodicals, Inc.
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Butin 7 3 4 trihydroxydihydroflavone reduces oxidative stress induced cell death via inhibition of the mitochondria dependent apoptotic pathway
International Journal of Molecular Sciences, 2011Co-Authors: Rui Zhang, Sungwook Chae, Mei Jing Piao, Hee Sun Kim, Ki Cheon Kim, Hye Sun Kim, In Kyung Lee, Areum Kim, Jin Won HyunAbstract:Recently, we demonstrated that Butin (7,3',4'-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H(2)O(2))-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of Butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H(2)O(2)-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3. Furthermore, the anti-apoptotic effect of Butin was exerted via inhibition of mitogen-activated protein kinase kinase-4, c-Jun NH(2)-terminal kinase (JNK) and activator protein-1 cascades induced by H(2)O(2) treatment. Finally, Butin exhibited protective effects against H(2)O(2)-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G(1) hypodiploid cells and DNA fragmentation. Taken together, the protective effects of Butin against H(2)O(2)-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathway.
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Butin (7,3′,4′-Trihydroxydihydroflavone) Reduces Oxidative Stress-Induced Cell Death via Inhibition of the Mitochondria-Dependent Apoptotic Pathway
MDPI AG, 2011Co-Authors: Jin Won Hyun, Rui Zhang, Sungwook Chae, Mei Jing Piao, Hee Sun Kim, Ki Cheon Kim, Areum Daseul Kim, Hye Sun Kim, In Kyung LeeAbstract:Recently, we demonstrated that Butin (7,3′,4′-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H2O2)-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of Butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H2O2-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3. Furthermore, the anti-apoptotic effect of Butin was exerted via inhibition of mitogen-activated protein kinase kinase-4, c-Jun NH2-terminal kinase (JNK) and activator protein-1 cascades induced by H2O2 treatment. Finally, Butin exhibited protective effects against H2O2-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G1 hypodiploid cells and DNA fragmentation. Taken together, the protective effects of Butin against H2O2-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathwa
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Butin reduces oxidative stress induced mitochondrial dysfunction via scavenging of reactive oxygen species
Food and Chemical Toxicology, 2010Co-Authors: Rui Zhang, Sungwook Chae, Kyoung Ah Kang, Mei Jing Piao, In Kyung Lee, Weon Young Chang, Young Hee Maeng, Bum Joon Kim, Jin Won HyunAbstract:Abstract This study investigated the cytoprotective effect of Butin, a flavonoid, on hydrogen peroxide (H2O2)-induced mitochondrial dysfunction. Electron spin resonance (ESR) spectrometry revealed Butin’s significant scavenging effects on superoxide radicals and hydroxyl radicals. When H2O2 was used to induce an increase in mitochondrial reactive oxygen species (ROS) in Chinese hamster lung fibroblast (V79-4) cells, Butin treatment decreased high level of ROS. Butin also attenuated intracellular Ca2+ levels that have been induced by H2O2. Furthermore, Butin recovered ATP levels and succinate dehydrogenase activity that had been decreased by H2O2 treatment. We conclude these results suggest Butin decreased mitochondrial ROS accumulation, balanced intracellular Ca2+ levels, and improved mitochondrial energy production, thus recovering mitochondrial function.
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butein induces g2 m phase arrest and apoptosis in human hepatoma cancer cells through ros generation
Cancer Letters, 2010Co-Authors: Dongoh Moon, Jin Won Hyun, Weon Young Chang, Munock Kim, Yung Hyun Choi, Giyoung KimAbstract:We investigated the molecular effects of 3,4,2',4'-tetrahydroxychalcone (butein) treatment in two human hepatoma cancer cell lines-HepG2 and Hep3B. Butein treatment inhibited cancer cell growth by inducing G(2)/M phase arrest and apoptosis. Butein-induced G(2)/M phase arrest was associated with increased ATM, Chk1, and Chk2 phosphorylations and reduced cdc25C levels. Additionally, butein treatment enhanced inactivated phospho-Cdc2 levels, reduced Cdc2 kinase activity, and generated reactive oxygen species (ROS) that was accompanied by JNK activation. The extent of butein-induced G(2)/M phase arrest significantly decreased following pretreatment with N-acetyl-l-cysteine or glutathione and following JNK phosphorylation reduction by SP600125. Both N-acetyl-l-cysteine and glutathione also decreased butein-mediated apoptosis. Taken together, these results imply a critical role of ROS and JNK in the anticancer effects of butein.
Rui Zhang - One of the best experts on this subject based on the ideXlab platform.
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the cytoprotective effect of Butin against oxidative stress is mediated by the up regulation of manganese superoxide dismutase expression through a pi3k akt nrf2 dependent pathway
Journal of Cellular Biochemistry, 2012Co-Authors: Rui Zhang, Sungwook Chae, Jun Hwa Lee, Jin Won HyunAbstract:Butin (7,3′,4′-trihydroxydihydroflavone), a flavonoid with antioxidant activity, was recently reported to protect cells against H2O2-induced apoptosis, oxidative DNA damage and oxidative mitochondrial dysfunction. The objective of the present study was to elucidate the mechanism by which Butin protects mitochondria. The antioxidant function of manganese superoxide dismutase (Mn SOD) is important in preventing oxidative stress. While exposure to H2O2 reduced the expression of Mn SOD in Chinese hamster lung fibroblast (V79-4), the addition of Butin restored Mn SOD expression at both the mRNA and protein levels, resulting in increased Mn SOD activity. The transcription factor NF-E2-related factor 2 (Nrf2) regulates Mn SOD gene expression by binding to the antioxidant responsive element (ARE). Butin enhanced the nuclear translocation and ARE-binding activity of Nrf2, which was decreased by H2O2. The siRNA-mediated knockdown of Nrf2 attenuated Butin-induced Mn SOD expression and activity. Further, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB, Akt) contributed to the ARE-driven Mn SOD expression. Butin activated PI3K/Akt and exposure to either LY294002 (a PI3K inhibitor), Akt inhibitor IV (an Akt-specific inhibitor), or Akt siRNA suppressed the Butin-induced activation of Nrf2, resulting in decreased Mn SOD expression and activity. Finally, the cytoprotective effect of Butin against H2O2-induced cell damage was suppressed by the siRNA-mediated knockdown of Mn SOD. These studies demonstrate that Butin attenuates oxidative stress by activating Nrf2-mediated Mn SOD induction via the PI3K/Akt signaling pathway. J. Cell. Biochem. 113: 1987–1997, 2012. © 2012 Wiley Periodicals, Inc.
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Butin 7 3 4 trihydroxydihydroflavone reduces oxidative stress induced cell death via inhibition of the mitochondria dependent apoptotic pathway
International Journal of Molecular Sciences, 2011Co-Authors: Rui Zhang, Sungwook Chae, Mei Jing Piao, Hee Sun Kim, Ki Cheon Kim, Hye Sun Kim, In Kyung Lee, Areum Kim, Jin Won HyunAbstract:Recently, we demonstrated that Butin (7,3',4'-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H(2)O(2))-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of Butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H(2)O(2)-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3. Furthermore, the anti-apoptotic effect of Butin was exerted via inhibition of mitogen-activated protein kinase kinase-4, c-Jun NH(2)-terminal kinase (JNK) and activator protein-1 cascades induced by H(2)O(2) treatment. Finally, Butin exhibited protective effects against H(2)O(2)-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G(1) hypodiploid cells and DNA fragmentation. Taken together, the protective effects of Butin against H(2)O(2)-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathway.
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Butin (7,3′,4′-Trihydroxydihydroflavone) Reduces Oxidative Stress-Induced Cell Death via Inhibition of the Mitochondria-Dependent Apoptotic Pathway
MDPI AG, 2011Co-Authors: Jin Won Hyun, Rui Zhang, Sungwook Chae, Mei Jing Piao, Hee Sun Kim, Ki Cheon Kim, Areum Daseul Kim, Hye Sun Kim, In Kyung LeeAbstract:Recently, we demonstrated that Butin (7,3′,4′-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H2O2)-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of Butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H2O2-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3. Furthermore, the anti-apoptotic effect of Butin was exerted via inhibition of mitogen-activated protein kinase kinase-4, c-Jun NH2-terminal kinase (JNK) and activator protein-1 cascades induced by H2O2 treatment. Finally, Butin exhibited protective effects against H2O2-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G1 hypodiploid cells and DNA fragmentation. Taken together, the protective effects of Butin against H2O2-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathwa
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Butin reduces oxidative stress induced mitochondrial dysfunction via scavenging of reactive oxygen species
Food and Chemical Toxicology, 2010Co-Authors: Rui Zhang, Sungwook Chae, Kyoung Ah Kang, Mei Jing Piao, In Kyung Lee, Weon Young Chang, Young Hee Maeng, Bum Joon Kim, Jin Won HyunAbstract:Abstract This study investigated the cytoprotective effect of Butin, a flavonoid, on hydrogen peroxide (H2O2)-induced mitochondrial dysfunction. Electron spin resonance (ESR) spectrometry revealed Butin’s significant scavenging effects on superoxide radicals and hydroxyl radicals. When H2O2 was used to induce an increase in mitochondrial reactive oxygen species (ROS) in Chinese hamster lung fibroblast (V79-4) cells, Butin treatment decreased high level of ROS. Butin also attenuated intracellular Ca2+ levels that have been induced by H2O2. Furthermore, Butin recovered ATP levels and succinate dehydrogenase activity that had been decreased by H2O2 treatment. We conclude these results suggest Butin decreased mitochondrial ROS accumulation, balanced intracellular Ca2+ levels, and improved mitochondrial energy production, thus recovering mitochondrial function.
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Butin decreases oxidative stress induced 8 hydroxy 2 deoxyguanosine levels via activation of oxoguanine glycosylase 1
Chemico-Biological Interactions, 2009Co-Authors: Kyoung Ah Kang, Rui Zhang, Sungwook Chae, Mei Jing Piao, Hee Sun Kim, Jung Hee Lee, Ho Jin You, Jin Won HyunAbstract:In response to oxidative DNA base damage, oxoguanine glycosylase 1 (OGG1), in a base-excision repair (BER) pathway in mammals, plays a vital role in the repair of 8-hydroxy-2'-deoxyguanosine (8-OHdG), which is a reliable marker of reactive oxygen species (ROS)-induced DNA base modification and contributes to the pathologic process of cancer. Recently, we have shown that Butin (7,3',4'-trihydroxydihydroflavone) protects cells against hydrogen peroxide (H2O2)-induced damage of cellular components including DNA. In the present study, we examined the possible protective effect of Butin on oxidative stress-induced DNA base modification, especially 8-OHdG. Hydrogen peroxide significantly increased the level of 8-OHdG, which was detected by 8-OHdG ELISA and confocal microscopy, but Butin decreased this level. Suppression of 8-OHdG formation by Butin was related to the enhanced mRNA and protein expression of OGG1, which was detected by RT-PCR and Western blot analysis. Butin also increased the transcriptional activity of OGG1, which was suppressed by H2O2 treatment; this transcriptional activity was detected by OGG1 promoter luciferase assay. Butin enhanced the expression of phosphorylated Akt (active form of Akt), a regulator of OGG1, which was decreased by H2O2 treatment. A PI3K-specific inhibitor, LY294002, abolished the phosphorylated Akt and OGG1 expressions induced by Butin, suggesting that OGG1 induction by Butin involves the PI3K/Akt pathway.
Sungwook Chae - One of the best experts on this subject based on the ideXlab platform.
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the cytoprotective effect of Butin against oxidative stress is mediated by the up regulation of manganese superoxide dismutase expression through a pi3k akt nrf2 dependent pathway
Journal of Cellular Biochemistry, 2012Co-Authors: Rui Zhang, Sungwook Chae, Jun Hwa Lee, Jin Won HyunAbstract:Butin (7,3′,4′-trihydroxydihydroflavone), a flavonoid with antioxidant activity, was recently reported to protect cells against H2O2-induced apoptosis, oxidative DNA damage and oxidative mitochondrial dysfunction. The objective of the present study was to elucidate the mechanism by which Butin protects mitochondria. The antioxidant function of manganese superoxide dismutase (Mn SOD) is important in preventing oxidative stress. While exposure to H2O2 reduced the expression of Mn SOD in Chinese hamster lung fibroblast (V79-4), the addition of Butin restored Mn SOD expression at both the mRNA and protein levels, resulting in increased Mn SOD activity. The transcription factor NF-E2-related factor 2 (Nrf2) regulates Mn SOD gene expression by binding to the antioxidant responsive element (ARE). Butin enhanced the nuclear translocation and ARE-binding activity of Nrf2, which was decreased by H2O2. The siRNA-mediated knockdown of Nrf2 attenuated Butin-induced Mn SOD expression and activity. Further, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB, Akt) contributed to the ARE-driven Mn SOD expression. Butin activated PI3K/Akt and exposure to either LY294002 (a PI3K inhibitor), Akt inhibitor IV (an Akt-specific inhibitor), or Akt siRNA suppressed the Butin-induced activation of Nrf2, resulting in decreased Mn SOD expression and activity. Finally, the cytoprotective effect of Butin against H2O2-induced cell damage was suppressed by the siRNA-mediated knockdown of Mn SOD. These studies demonstrate that Butin attenuates oxidative stress by activating Nrf2-mediated Mn SOD induction via the PI3K/Akt signaling pathway. J. Cell. Biochem. 113: 1987–1997, 2012. © 2012 Wiley Periodicals, Inc.
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Butin 7 3 4 trihydroxydihydroflavone reduces oxidative stress induced cell death via inhibition of the mitochondria dependent apoptotic pathway
International Journal of Molecular Sciences, 2011Co-Authors: Rui Zhang, Sungwook Chae, Mei Jing Piao, Hee Sun Kim, Ki Cheon Kim, Hye Sun Kim, In Kyung Lee, Areum Kim, Jin Won HyunAbstract:Recently, we demonstrated that Butin (7,3',4'-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H(2)O(2))-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of Butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H(2)O(2)-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3. Furthermore, the anti-apoptotic effect of Butin was exerted via inhibition of mitogen-activated protein kinase kinase-4, c-Jun NH(2)-terminal kinase (JNK) and activator protein-1 cascades induced by H(2)O(2) treatment. Finally, Butin exhibited protective effects against H(2)O(2)-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G(1) hypodiploid cells and DNA fragmentation. Taken together, the protective effects of Butin against H(2)O(2)-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathway.
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Butin (7,3′,4′-Trihydroxydihydroflavone) Reduces Oxidative Stress-Induced Cell Death via Inhibition of the Mitochondria-Dependent Apoptotic Pathway
MDPI AG, 2011Co-Authors: Jin Won Hyun, Rui Zhang, Sungwook Chae, Mei Jing Piao, Hee Sun Kim, Ki Cheon Kim, Areum Daseul Kim, Hye Sun Kim, In Kyung LeeAbstract:Recently, we demonstrated that Butin (7,3′,4′-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H2O2)-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of Butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H2O2-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3. Furthermore, the anti-apoptotic effect of Butin was exerted via inhibition of mitogen-activated protein kinase kinase-4, c-Jun NH2-terminal kinase (JNK) and activator protein-1 cascades induced by H2O2 treatment. Finally, Butin exhibited protective effects against H2O2-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G1 hypodiploid cells and DNA fragmentation. Taken together, the protective effects of Butin against H2O2-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathwa
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Butin reduces oxidative stress induced mitochondrial dysfunction via scavenging of reactive oxygen species
Food and Chemical Toxicology, 2010Co-Authors: Rui Zhang, Sungwook Chae, Kyoung Ah Kang, Mei Jing Piao, In Kyung Lee, Weon Young Chang, Young Hee Maeng, Bum Joon Kim, Jin Won HyunAbstract:Abstract This study investigated the cytoprotective effect of Butin, a flavonoid, on hydrogen peroxide (H2O2)-induced mitochondrial dysfunction. Electron spin resonance (ESR) spectrometry revealed Butin’s significant scavenging effects on superoxide radicals and hydroxyl radicals. When H2O2 was used to induce an increase in mitochondrial reactive oxygen species (ROS) in Chinese hamster lung fibroblast (V79-4) cells, Butin treatment decreased high level of ROS. Butin also attenuated intracellular Ca2+ levels that have been induced by H2O2. Furthermore, Butin recovered ATP levels and succinate dehydrogenase activity that had been decreased by H2O2 treatment. We conclude these results suggest Butin decreased mitochondrial ROS accumulation, balanced intracellular Ca2+ levels, and improved mitochondrial energy production, thus recovering mitochondrial function.
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Butin decreases oxidative stress induced 8 hydroxy 2 deoxyguanosine levels via activation of oxoguanine glycosylase 1
Chemico-Biological Interactions, 2009Co-Authors: Kyoung Ah Kang, Rui Zhang, Sungwook Chae, Mei Jing Piao, Hee Sun Kim, Jung Hee Lee, Ho Jin You, Jin Won HyunAbstract:In response to oxidative DNA base damage, oxoguanine glycosylase 1 (OGG1), in a base-excision repair (BER) pathway in mammals, plays a vital role in the repair of 8-hydroxy-2'-deoxyguanosine (8-OHdG), which is a reliable marker of reactive oxygen species (ROS)-induced DNA base modification and contributes to the pathologic process of cancer. Recently, we have shown that Butin (7,3',4'-trihydroxydihydroflavone) protects cells against hydrogen peroxide (H2O2)-induced damage of cellular components including DNA. In the present study, we examined the possible protective effect of Butin on oxidative stress-induced DNA base modification, especially 8-OHdG. Hydrogen peroxide significantly increased the level of 8-OHdG, which was detected by 8-OHdG ELISA and confocal microscopy, but Butin decreased this level. Suppression of 8-OHdG formation by Butin was related to the enhanced mRNA and protein expression of OGG1, which was detected by RT-PCR and Western blot analysis. Butin also increased the transcriptional activity of OGG1, which was suppressed by H2O2 treatment; this transcriptional activity was detected by OGG1 promoter luciferase assay. Butin enhanced the expression of phosphorylated Akt (active form of Akt), a regulator of OGG1, which was decreased by H2O2 treatment. A PI3K-specific inhibitor, LY294002, abolished the phosphorylated Akt and OGG1 expressions induced by Butin, suggesting that OGG1 induction by Butin involves the PI3K/Akt pathway.
Hye Hyun Yoo - One of the best experts on this subject based on the ideXlab platform.
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inhibitory effect of rhus verniciflua stokes extract on human aromatase activity Butin is its major bioactive component
Bioorganic & Medicinal Chemistry Letters, 2014Co-Authors: Myeong Hyeon Park, In Sook Kim, Suna Kim, Cheol Yi Hong, Misook Dong, Hye Hyun YooAbstract:Rhus verniciflua Stokes has been used as a traditional herbal medicine in Asia. In this study, the effect of R. verniciflua extract on human aromatase (cytochrome P450 19, CYP19) activity was investigated to elucidate the mechanism for the effect of R. verniciflua extract on androgen hormone levels. Androstenedione was used as a substrate and incubated with R. verniciflua extract in cDNA-expressed CYP19 supersomes in the presence of NADPH, and estrone formation was measured using liquid chromatography-tandem mass spectrometry. R. verniciflua extract was assessed at concentrations of 10-1000 μg/mL. The resulting data showed that R. verniciflua extract inhibited CYP19-mediated estrone formation in a concentration-dependent manner with an IC50 value of 136 μg/mL. Subsequently, polyphenolic compounds from R. verniciflua extract were tested to identify the ingredients responsible for the aromatase inhibitory effects by R. verniciflua extract. As a result, Butin showed aromatase inhibitory effect in a concentration-dependent manner with an IC50 value of 9.6 μM, whereas the inhibition by other compounds was negligible. These results suggest that R. verniciflua extract could modulate androgen hormone levels via the inhibition of CYP19 activity and Butin is a major ingredient responsible for this activity.
Mei Jing Piao - One of the best experts on this subject based on the ideXlab platform.
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Butin 7 3 4 trihydroxydihydroflavone reduces oxidative stress induced cell death via inhibition of the mitochondria dependent apoptotic pathway
International Journal of Molecular Sciences, 2011Co-Authors: Rui Zhang, Sungwook Chae, Mei Jing Piao, Hee Sun Kim, Ki Cheon Kim, Hye Sun Kim, In Kyung Lee, Areum Kim, Jin Won HyunAbstract:Recently, we demonstrated that Butin (7,3',4'-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H(2)O(2))-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of Butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H(2)O(2)-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3. Furthermore, the anti-apoptotic effect of Butin was exerted via inhibition of mitogen-activated protein kinase kinase-4, c-Jun NH(2)-terminal kinase (JNK) and activator protein-1 cascades induced by H(2)O(2) treatment. Finally, Butin exhibited protective effects against H(2)O(2)-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G(1) hypodiploid cells and DNA fragmentation. Taken together, the protective effects of Butin against H(2)O(2)-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathway.
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Butin (7,3′,4′-Trihydroxydihydroflavone) Reduces Oxidative Stress-Induced Cell Death via Inhibition of the Mitochondria-Dependent Apoptotic Pathway
MDPI AG, 2011Co-Authors: Jin Won Hyun, Rui Zhang, Sungwook Chae, Mei Jing Piao, Hee Sun Kim, Ki Cheon Kim, Areum Daseul Kim, Hye Sun Kim, In Kyung LeeAbstract:Recently, we demonstrated that Butin (7,3′,4′-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H2O2)-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of Butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H2O2-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3. Furthermore, the anti-apoptotic effect of Butin was exerted via inhibition of mitogen-activated protein kinase kinase-4, c-Jun NH2-terminal kinase (JNK) and activator protein-1 cascades induced by H2O2 treatment. Finally, Butin exhibited protective effects against H2O2-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G1 hypodiploid cells and DNA fragmentation. Taken together, the protective effects of Butin against H2O2-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathwa
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Butin reduces oxidative stress induced mitochondrial dysfunction via scavenging of reactive oxygen species
Food and Chemical Toxicology, 2010Co-Authors: Rui Zhang, Sungwook Chae, Kyoung Ah Kang, Mei Jing Piao, In Kyung Lee, Weon Young Chang, Young Hee Maeng, Bum Joon Kim, Jin Won HyunAbstract:Abstract This study investigated the cytoprotective effect of Butin, a flavonoid, on hydrogen peroxide (H2O2)-induced mitochondrial dysfunction. Electron spin resonance (ESR) spectrometry revealed Butin’s significant scavenging effects on superoxide radicals and hydroxyl radicals. When H2O2 was used to induce an increase in mitochondrial reactive oxygen species (ROS) in Chinese hamster lung fibroblast (V79-4) cells, Butin treatment decreased high level of ROS. Butin also attenuated intracellular Ca2+ levels that have been induced by H2O2. Furthermore, Butin recovered ATP levels and succinate dehydrogenase activity that had been decreased by H2O2 treatment. We conclude these results suggest Butin decreased mitochondrial ROS accumulation, balanced intracellular Ca2+ levels, and improved mitochondrial energy production, thus recovering mitochondrial function.
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Butin decreases oxidative stress induced 8 hydroxy 2 deoxyguanosine levels via activation of oxoguanine glycosylase 1
Chemico-Biological Interactions, 2009Co-Authors: Kyoung Ah Kang, Rui Zhang, Sungwook Chae, Mei Jing Piao, Hee Sun Kim, Jung Hee Lee, Ho Jin You, Jin Won HyunAbstract:In response to oxidative DNA base damage, oxoguanine glycosylase 1 (OGG1), in a base-excision repair (BER) pathway in mammals, plays a vital role in the repair of 8-hydroxy-2'-deoxyguanosine (8-OHdG), which is a reliable marker of reactive oxygen species (ROS)-induced DNA base modification and contributes to the pathologic process of cancer. Recently, we have shown that Butin (7,3',4'-trihydroxydihydroflavone) protects cells against hydrogen peroxide (H2O2)-induced damage of cellular components including DNA. In the present study, we examined the possible protective effect of Butin on oxidative stress-induced DNA base modification, especially 8-OHdG. Hydrogen peroxide significantly increased the level of 8-OHdG, which was detected by 8-OHdG ELISA and confocal microscopy, but Butin decreased this level. Suppression of 8-OHdG formation by Butin was related to the enhanced mRNA and protein expression of OGG1, which was detected by RT-PCR and Western blot analysis. Butin also increased the transcriptional activity of OGG1, which was suppressed by H2O2 treatment; this transcriptional activity was detected by OGG1 promoter luciferase assay. Butin enhanced the expression of phosphorylated Akt (active form of Akt), a regulator of OGG1, which was decreased by H2O2 treatment. A PI3K-specific inhibitor, LY294002, abolished the phosphorylated Akt and OGG1 expressions induced by Butin, suggesting that OGG1 induction by Butin involves the PI3K/Akt pathway.
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Protective effect of Butin against hydrogen peroxide-induced apoptosis by scavenging reactive oxygen species and activating antioxidant enzymes
Molecular and Cellular Biochemistry, 2008Co-Authors: Rui Zhang, Sungwook Chae, Kyoung Ah Kang, Mei Jing Piao, Dong Ok Ko, Zhi Hong Wang, Doek Bae Park, Jae Woo Park, Jin Won HyunAbstract:The antioxidant property of Butin was investigated for cytoprotective effect against H_2O_2-induced cell damage. This compound showed intracellular reactive oxygen species (ROS) scavenging, 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging, inhibition of lipid peroxidation, and DNA damage. This radical scavenging activity of Butin protected cell damage exposed to H_2O_2. Also, Butin reduced the apoptotic cells induced by H_2O_2, as demonstrated by the decreased DNA fragmentation, apoptotic body formation, and caspase 3 activity. In addition, Butin restored the activity and protein expression of cellular antioxidant enzymes, superoxide dismutase (SOD), and catalase (CAT) in H_2O_2-treated cells. Taken together, these findings suggest that Butin protected cells against H_2O_2-induced cell damage via antioxidant property.
