Syringaresinol

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Takahiko Shimizu - One of the best experts on this subject based on the ideXlab platform.

  • Syringaresinol reverses age related skin atrophy by suppressing foxo3a mediated matrix metalloproteinase 2 activation in copper zinc superoxide dismutase deficient mice
    Journal of Investigative Dermatology, 2019
    Co-Authors: Juewon Kim, Si Young Cho, Toshihiko Toda, Kenji Watanabe, Shuichi Shibuya, Yusuke Ozawa, Naotaka Izuo, Dae Bang Seo, Koutaro Yokote, Takahiko Shimizu
    Abstract:

    Aging is characterized by accumulation of chronic and irreversible oxidative damage, chronic inflammation, and organ dysfunction. Superoxide dismutase (SOD) serves as a major enzyme for cellular superoxide radical metabolism and physiologically regulates cellular redox balance throughout the body. Copper/zinc superoxide dismutase–deficient (SOD1–/–) mice showed diverse phenotypes associated with enhanced oxidative damage in whole organs. Here, we found that oral treatment with Syringaresinol (also known as lirioresinol B), which is the active component in the berries of Korean ginseng (Panax ginseng C.A. Meyer), attenuated the age-related changes in Sod1–/– skin. Interestingly, Syringaresinol morphologically normalized skin atrophy in Sod1–/– mice and promoted fibroblast outgrowth from Sod1–/– skin in vitro. These protective effects were mediated by the suppression of matrix metalloproteinase-2 overproduction in Sod1–/– skin, but not by increased collagen expression. Syringaresinol also decreased the oxidative damage and the phosphorylation of FoxO3a protein, which was a transcriptional factor of matrix metalloproteinase–2, in Sod1–/– skin. These results strongly suggest that Syringaresinol regulates the FoxO3–matrix metalloproteinase-2 axis in oxidative damaged skin and exhibits beneficial effects on age-related skin involution in Sod1–/– mice.

  • Syringaresinol Reverses Age-Related Skin Atrophy by Suppressing FoxO3a-Mediated Matrix Metalloproteinase–2 Activation in Copper/Zinc Superoxide Dismutase–Deficient Mice
    The Journal of investigative dermatology, 2018
    Co-Authors: Juewon Kim, Si Young Cho, Toshihiko Toda, Kenji Watanabe, Shuichi Shibuya, Yusuke Ozawa, Naotaka Izuo, Dae Bang Seo, Koutaro Yokote, Takahiko Shimizu
    Abstract:

    Aging is characterized by accumulation of chronic and irreversible oxidative damage, chronic inflammation, and organ dysfunction. Superoxide dismutase (SOD) serves as a major enzyme for cellular superoxide radical metabolism and physiologically regulates cellular redox balance throughout the body. Copper/zinc superoxide dismutase–deficient (SOD1–/–) mice showed diverse phenotypes associated with enhanced oxidative damage in whole organs. Here, we found that oral treatment with Syringaresinol (also known as lirioresinol B), which is the active component in the berries of Korean ginseng (Panax ginseng C.A. Meyer), attenuated the age-related changes in Sod1–/– skin. Interestingly, Syringaresinol morphologically normalized skin atrophy in Sod1–/– mice and promoted fibroblast outgrowth from Sod1–/– skin in vitro. These protective effects were mediated by the suppression of matrix metalloproteinase-2 overproduction in Sod1–/– skin, but not by increased collagen expression. Syringaresinol also decreased the oxidative damage and the phosphorylation of FoxO3a protein, which was a transcriptional factor of matrix metalloproteinase–2, in Sod1–/– skin. These results strongly suggest that Syringaresinol regulates the FoxO3–matrix metalloproteinase-2 axis in oxidative damaged skin and exhibits beneficial effects on age-related skin involution in Sod1–/– mice.

  • Effects of Korean ginseng berry on skin antipigmentation and antiaging via FoxO3a activation.
    Journal of ginseng research, 2016
    Co-Authors: Juewon Kim, Si Young Cho, Dae Bang Seo, Takahiko Shimizu, Su Hwan Kim, Donghyun Cho, Sunmi Kim, Chan-woong Park, Jae Youl Cho, Song Seok Shin
    Abstract:

    Abstract Background The ginseng berry has various bioactivities, including antidiabetic, anticancer, antiinflammatory, and antioxidative properties. Moreover, we have revealed that the active antiaging component of the ginseng berry, Syringaresinol, has the ability to stimulate longevity via gene activation. Despite the many known beneficial effects of ginseng, its effects on skin aging are poorly understood. In this study, we investigated the effects of ginseng and the ginseng berry on one of the skin aging processes, melanogenesis, and age-related pigment lipofuscin accumulation, to elucidate the mechanism of action with respect to antiaging. Methods The human melanoma MNT1 cell line was treated with ginseng root extract, ginseng berry extract, or Syringaresinol. Then, the cells were analyzed using a melanin assay, and the tyrosinase activity was estimated. The Caenorhabditis elegans wild type N2 strain was used for the life span assay to analyze the antiaging effects of the samples. A lipofuscin fluorescence assay was performed during 10 passages with the Syringaresinol treatment. Results A 7-d treatment with ginseng berry extract reduced melanin accumulation and tyrosinase activity more than ginseng root extract. These results may be due to the active compound of the ginseng berry, Syringaresinol. The antimelanogenic activity was strongly coordinated with the activation of the longevity gene foxo3a . Moreover, the ginseng berry extract had more potent antiaging effects, caused a life span extension, and reduced lipofuscin accumulation. Conclusion Taken together, our results suggest that these antimelanogenic effects and antiaging effects of ginseng berry mediate the activation of antioxidation–FoxO3a signaling.

Juewon Kim - One of the best experts on this subject based on the ideXlab platform.

  • Syringaresinol reverses age related skin atrophy by suppressing foxo3a mediated matrix metalloproteinase 2 activation in copper zinc superoxide dismutase deficient mice
    Journal of Investigative Dermatology, 2019
    Co-Authors: Juewon Kim, Si Young Cho, Toshihiko Toda, Kenji Watanabe, Shuichi Shibuya, Yusuke Ozawa, Naotaka Izuo, Dae Bang Seo, Koutaro Yokote, Takahiko Shimizu
    Abstract:

    Aging is characterized by accumulation of chronic and irreversible oxidative damage, chronic inflammation, and organ dysfunction. Superoxide dismutase (SOD) serves as a major enzyme for cellular superoxide radical metabolism and physiologically regulates cellular redox balance throughout the body. Copper/zinc superoxide dismutase–deficient (SOD1–/–) mice showed diverse phenotypes associated with enhanced oxidative damage in whole organs. Here, we found that oral treatment with Syringaresinol (also known as lirioresinol B), which is the active component in the berries of Korean ginseng (Panax ginseng C.A. Meyer), attenuated the age-related changes in Sod1–/– skin. Interestingly, Syringaresinol morphologically normalized skin atrophy in Sod1–/– mice and promoted fibroblast outgrowth from Sod1–/– skin in vitro. These protective effects were mediated by the suppression of matrix metalloproteinase-2 overproduction in Sod1–/– skin, but not by increased collagen expression. Syringaresinol also decreased the oxidative damage and the phosphorylation of FoxO3a protein, which was a transcriptional factor of matrix metalloproteinase–2, in Sod1–/– skin. These results strongly suggest that Syringaresinol regulates the FoxO3–matrix metalloproteinase-2 axis in oxidative damaged skin and exhibits beneficial effects on age-related skin involution in Sod1–/– mice.

  • Syringaresinol Reverses Age-Related Skin Atrophy by Suppressing FoxO3a-Mediated Matrix Metalloproteinase–2 Activation in Copper/Zinc Superoxide Dismutase–Deficient Mice
    The Journal of investigative dermatology, 2018
    Co-Authors: Juewon Kim, Si Young Cho, Toshihiko Toda, Kenji Watanabe, Shuichi Shibuya, Yusuke Ozawa, Naotaka Izuo, Dae Bang Seo, Koutaro Yokote, Takahiko Shimizu
    Abstract:

    Aging is characterized by accumulation of chronic and irreversible oxidative damage, chronic inflammation, and organ dysfunction. Superoxide dismutase (SOD) serves as a major enzyme for cellular superoxide radical metabolism and physiologically regulates cellular redox balance throughout the body. Copper/zinc superoxide dismutase–deficient (SOD1–/–) mice showed diverse phenotypes associated with enhanced oxidative damage in whole organs. Here, we found that oral treatment with Syringaresinol (also known as lirioresinol B), which is the active component in the berries of Korean ginseng (Panax ginseng C.A. Meyer), attenuated the age-related changes in Sod1–/– skin. Interestingly, Syringaresinol morphologically normalized skin atrophy in Sod1–/– mice and promoted fibroblast outgrowth from Sod1–/– skin in vitro. These protective effects were mediated by the suppression of matrix metalloproteinase-2 overproduction in Sod1–/– skin, but not by increased collagen expression. Syringaresinol also decreased the oxidative damage and the phosphorylation of FoxO3a protein, which was a transcriptional factor of matrix metalloproteinase–2, in Sod1–/– skin. These results strongly suggest that Syringaresinol regulates the FoxO3–matrix metalloproteinase-2 axis in oxidative damaged skin and exhibits beneficial effects on age-related skin involution in Sod1–/– mice.

  • Effects of Korean ginseng berry on skin antipigmentation and antiaging via FoxO3a activation.
    Journal of ginseng research, 2016
    Co-Authors: Juewon Kim, Si Young Cho, Dae Bang Seo, Takahiko Shimizu, Su Hwan Kim, Donghyun Cho, Sunmi Kim, Chan-woong Park, Jae Youl Cho, Song Seok Shin
    Abstract:

    Abstract Background The ginseng berry has various bioactivities, including antidiabetic, anticancer, antiinflammatory, and antioxidative properties. Moreover, we have revealed that the active antiaging component of the ginseng berry, Syringaresinol, has the ability to stimulate longevity via gene activation. Despite the many known beneficial effects of ginseng, its effects on skin aging are poorly understood. In this study, we investigated the effects of ginseng and the ginseng berry on one of the skin aging processes, melanogenesis, and age-related pigment lipofuscin accumulation, to elucidate the mechanism of action with respect to antiaging. Methods The human melanoma MNT1 cell line was treated with ginseng root extract, ginseng berry extract, or Syringaresinol. Then, the cells were analyzed using a melanin assay, and the tyrosinase activity was estimated. The Caenorhabditis elegans wild type N2 strain was used for the life span assay to analyze the antiaging effects of the samples. A lipofuscin fluorescence assay was performed during 10 passages with the Syringaresinol treatment. Results A 7-d treatment with ginseng berry extract reduced melanin accumulation and tyrosinase activity more than ginseng root extract. These results may be due to the active compound of the ginseng berry, Syringaresinol. The antimelanogenic activity was strongly coordinated with the activation of the longevity gene foxo3a . Moreover, the ginseng berry extract had more potent antiaging effects, caused a life span extension, and reduced lipofuscin accumulation. Conclusion Taken together, our results suggest that these antimelanogenic effects and antiaging effects of ginseng berry mediate the activation of antioxidation–FoxO3a signaling.

  • Syringaresinol protects against hypoxia reoxygenation induced cardiomyocytes injury and death by destabilization of hif 1α in a foxo3 dependent mechanism
    Oncotarget, 2015
    Co-Authors: Si Young Cho, Sang Jun Lee, Juewon Kim, Miook Cho, Matt Kaeberlein, Yousin Suh
    Abstract:

    // Siyoung Cho 1 , Miook Cho 2 , Juewon Kim 1 , Matt Kaeberlein 3 , Sang Jun Lee 1 and Yousin Suh 2,4,5 1 R&D Unit, Amorepacific Corporation, Yongin-si, Gyeonggi-do, Korea 2 Department of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA 3 Department of Pathology, University of Washington, Seattle, WA, USA 4 Department of Medicine, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, NY, USA 5 Institute for Aging Research, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, NY, USA Correspondence: Sang Jun Lee, email: // Yousin Suh, email: // Keywords : HIF-1α, Syringaresinol, FOXO3, ischemia/reperfusion, hypoxia/reoxygenation, cardiomyocytes Received : August 28, 2014 Accepted : November 06, 2014 Published : November 06, 2014 Abstract Hypoxia-inducible factor 1 (HIF-1) is a master regulator of hypoxic response and has been a prime therapeutic target for ischemia/reperfusion (I/R)-derived myocardial dysfunction and tissue damage. There is also increasing evidence that HIF-1 plays a central role in regulating aging, both through interactions with key longevity factors including Sirtuins and mTOR, as well as by directly promoting longevity in Caenorhabditis elegans .We investigated a novel function and the underlying mechanism of Syringaresinol, a lignan compound, in modulation of HIF-1 and protection against cellular damage and death in a cardiomyocyte model of I/R injury. Syringaresinol caused destabilization of HIF-1α following H/R and then protected against hypoxia/reoxygenation (H/R)-induced cellular damage, apoptosis, and mitochondrial dysfunction in a dose-dependent manner. Knock-down of FOXO3 by specific siRNAs completely abolished the ability of Syringaresinol to inhibit HIF-1 stabilization and apoptosis caused by H/R. Syringaresinol stimulated the nuclear localization and activity of FOXO3 leading to increased expression of antioxidant genes and decreased levels of reactive oxygen species (ROS) following H/R. Our results provide a new mechanistic insight into a functional role of Syringaresinol against H/R-induced cardiomyocyte injury and death. The degradation of HIF-1α through activation of FOXO3 is a potential therapeutic strategy for ischemia-related diseases.

  • Syringaresinol protects against hypoxia/reoxygenation-induced cardiomyocytes injury and death by destabilization of HIF-1α in a FOXO3-dependent mechanism
    Oncotarget, 2014
    Co-Authors: Si Young Cho, Sang Jun Lee, Juewon Kim, Miook Cho, Matt Kaeberlein, Yousin Suh
    Abstract:

    // Siyoung Cho 1 , Miook Cho 2 , Juewon Kim 1 , Matt Kaeberlein 3 , Sang Jun Lee 1 and Yousin Suh 2,4,5 1 R&D Unit, Amorepacific Corporation, Yongin-si, Gyeonggi-do, Korea 2 Department of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA 3 Department of Pathology, University of Washington, Seattle, WA, USA 4 Department of Medicine, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, NY, USA 5 Institute for Aging Research, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, NY, USA Correspondence: Sang Jun Lee, email: // Yousin Suh, email: // Keywords : HIF-1α, Syringaresinol, FOXO3, ischemia/reperfusion, hypoxia/reoxygenation, cardiomyocytes Received : August 28, 2014 Accepted : November 06, 2014 Published : November 06, 2014 Abstract Hypoxia-inducible factor 1 (HIF-1) is a master regulator of hypoxic response and has been a prime therapeutic target for ischemia/reperfusion (I/R)-derived myocardial dysfunction and tissue damage. There is also increasing evidence that HIF-1 plays a central role in regulating aging, both through interactions with key longevity factors including Sirtuins and mTOR, as well as by directly promoting longevity in Caenorhabditis elegans .We investigated a novel function and the underlying mechanism of Syringaresinol, a lignan compound, in modulation of HIF-1 and protection against cellular damage and death in a cardiomyocyte model of I/R injury. Syringaresinol caused destabilization of HIF-1α following H/R and then protected against hypoxia/reoxygenation (H/R)-induced cellular damage, apoptosis, and mitochondrial dysfunction in a dose-dependent manner. Knock-down of FOXO3 by specific siRNAs completely abolished the ability of Syringaresinol to inhibit HIF-1 stabilization and apoptosis caused by H/R. Syringaresinol stimulated the nuclear localization and activity of FOXO3 leading to increased expression of antioxidant genes and decreased levels of reactive oxygen species (ROS) following H/R. Our results provide a new mechanistic insight into a functional role of Syringaresinol against H/R-induced cardiomyocyte injury and death. The degradation of HIF-1α through activation of FOXO3 is a potential therapeutic strategy for ischemia-related diseases.

Si Young Cho - One of the best experts on this subject based on the ideXlab platform.

  • Syringaresinol reverses age related skin atrophy by suppressing foxo3a mediated matrix metalloproteinase 2 activation in copper zinc superoxide dismutase deficient mice
    Journal of Investigative Dermatology, 2019
    Co-Authors: Juewon Kim, Si Young Cho, Toshihiko Toda, Kenji Watanabe, Shuichi Shibuya, Yusuke Ozawa, Naotaka Izuo, Dae Bang Seo, Koutaro Yokote, Takahiko Shimizu
    Abstract:

    Aging is characterized by accumulation of chronic and irreversible oxidative damage, chronic inflammation, and organ dysfunction. Superoxide dismutase (SOD) serves as a major enzyme for cellular superoxide radical metabolism and physiologically regulates cellular redox balance throughout the body. Copper/zinc superoxide dismutase–deficient (SOD1–/–) mice showed diverse phenotypes associated with enhanced oxidative damage in whole organs. Here, we found that oral treatment with Syringaresinol (also known as lirioresinol B), which is the active component in the berries of Korean ginseng (Panax ginseng C.A. Meyer), attenuated the age-related changes in Sod1–/– skin. Interestingly, Syringaresinol morphologically normalized skin atrophy in Sod1–/– mice and promoted fibroblast outgrowth from Sod1–/– skin in vitro. These protective effects were mediated by the suppression of matrix metalloproteinase-2 overproduction in Sod1–/– skin, but not by increased collagen expression. Syringaresinol also decreased the oxidative damage and the phosphorylation of FoxO3a protein, which was a transcriptional factor of matrix metalloproteinase–2, in Sod1–/– skin. These results strongly suggest that Syringaresinol regulates the FoxO3–matrix metalloproteinase-2 axis in oxidative damaged skin and exhibits beneficial effects on age-related skin involution in Sod1–/– mice.

  • Syringaresinol Reverses Age-Related Skin Atrophy by Suppressing FoxO3a-Mediated Matrix Metalloproteinase–2 Activation in Copper/Zinc Superoxide Dismutase–Deficient Mice
    The Journal of investigative dermatology, 2018
    Co-Authors: Juewon Kim, Si Young Cho, Toshihiko Toda, Kenji Watanabe, Shuichi Shibuya, Yusuke Ozawa, Naotaka Izuo, Dae Bang Seo, Koutaro Yokote, Takahiko Shimizu
    Abstract:

    Aging is characterized by accumulation of chronic and irreversible oxidative damage, chronic inflammation, and organ dysfunction. Superoxide dismutase (SOD) serves as a major enzyme for cellular superoxide radical metabolism and physiologically regulates cellular redox balance throughout the body. Copper/zinc superoxide dismutase–deficient (SOD1–/–) mice showed diverse phenotypes associated with enhanced oxidative damage in whole organs. Here, we found that oral treatment with Syringaresinol (also known as lirioresinol B), which is the active component in the berries of Korean ginseng (Panax ginseng C.A. Meyer), attenuated the age-related changes in Sod1–/– skin. Interestingly, Syringaresinol morphologically normalized skin atrophy in Sod1–/– mice and promoted fibroblast outgrowth from Sod1–/– skin in vitro. These protective effects were mediated by the suppression of matrix metalloproteinase-2 overproduction in Sod1–/– skin, but not by increased collagen expression. Syringaresinol also decreased the oxidative damage and the phosphorylation of FoxO3a protein, which was a transcriptional factor of matrix metalloproteinase–2, in Sod1–/– skin. These results strongly suggest that Syringaresinol regulates the FoxO3–matrix metalloproteinase-2 axis in oxidative damaged skin and exhibits beneficial effects on age-related skin involution in Sod1–/– mice.

  • Effects of Korean ginseng berry on skin antipigmentation and antiaging via FoxO3a activation.
    Journal of ginseng research, 2016
    Co-Authors: Juewon Kim, Si Young Cho, Dae Bang Seo, Takahiko Shimizu, Su Hwan Kim, Donghyun Cho, Sunmi Kim, Chan-woong Park, Jae Youl Cho, Song Seok Shin
    Abstract:

    Abstract Background The ginseng berry has various bioactivities, including antidiabetic, anticancer, antiinflammatory, and antioxidative properties. Moreover, we have revealed that the active antiaging component of the ginseng berry, Syringaresinol, has the ability to stimulate longevity via gene activation. Despite the many known beneficial effects of ginseng, its effects on skin aging are poorly understood. In this study, we investigated the effects of ginseng and the ginseng berry on one of the skin aging processes, melanogenesis, and age-related pigment lipofuscin accumulation, to elucidate the mechanism of action with respect to antiaging. Methods The human melanoma MNT1 cell line was treated with ginseng root extract, ginseng berry extract, or Syringaresinol. Then, the cells were analyzed using a melanin assay, and the tyrosinase activity was estimated. The Caenorhabditis elegans wild type N2 strain was used for the life span assay to analyze the antiaging effects of the samples. A lipofuscin fluorescence assay was performed during 10 passages with the Syringaresinol treatment. Results A 7-d treatment with ginseng berry extract reduced melanin accumulation and tyrosinase activity more than ginseng root extract. These results may be due to the active compound of the ginseng berry, Syringaresinol. The antimelanogenic activity was strongly coordinated with the activation of the longevity gene foxo3a . Moreover, the ginseng berry extract had more potent antiaging effects, caused a life span extension, and reduced lipofuscin accumulation. Conclusion Taken together, our results suggest that these antimelanogenic effects and antiaging effects of ginseng berry mediate the activation of antioxidation–FoxO3a signaling.

  • Syringaresinol protects against hypoxia reoxygenation induced cardiomyocytes injury and death by destabilization of hif 1α in a foxo3 dependent mechanism
    Oncotarget, 2015
    Co-Authors: Si Young Cho, Sang Jun Lee, Juewon Kim, Miook Cho, Matt Kaeberlein, Yousin Suh
    Abstract:

    // Siyoung Cho 1 , Miook Cho 2 , Juewon Kim 1 , Matt Kaeberlein 3 , Sang Jun Lee 1 and Yousin Suh 2,4,5 1 R&D Unit, Amorepacific Corporation, Yongin-si, Gyeonggi-do, Korea 2 Department of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA 3 Department of Pathology, University of Washington, Seattle, WA, USA 4 Department of Medicine, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, NY, USA 5 Institute for Aging Research, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, NY, USA Correspondence: Sang Jun Lee, email: // Yousin Suh, email: // Keywords : HIF-1α, Syringaresinol, FOXO3, ischemia/reperfusion, hypoxia/reoxygenation, cardiomyocytes Received : August 28, 2014 Accepted : November 06, 2014 Published : November 06, 2014 Abstract Hypoxia-inducible factor 1 (HIF-1) is a master regulator of hypoxic response and has been a prime therapeutic target for ischemia/reperfusion (I/R)-derived myocardial dysfunction and tissue damage. There is also increasing evidence that HIF-1 plays a central role in regulating aging, both through interactions with key longevity factors including Sirtuins and mTOR, as well as by directly promoting longevity in Caenorhabditis elegans .We investigated a novel function and the underlying mechanism of Syringaresinol, a lignan compound, in modulation of HIF-1 and protection against cellular damage and death in a cardiomyocyte model of I/R injury. Syringaresinol caused destabilization of HIF-1α following H/R and then protected against hypoxia/reoxygenation (H/R)-induced cellular damage, apoptosis, and mitochondrial dysfunction in a dose-dependent manner. Knock-down of FOXO3 by specific siRNAs completely abolished the ability of Syringaresinol to inhibit HIF-1 stabilization and apoptosis caused by H/R. Syringaresinol stimulated the nuclear localization and activity of FOXO3 leading to increased expression of antioxidant genes and decreased levels of reactive oxygen species (ROS) following H/R. Our results provide a new mechanistic insight into a functional role of Syringaresinol against H/R-induced cardiomyocyte injury and death. The degradation of HIF-1α through activation of FOXO3 is a potential therapeutic strategy for ischemia-related diseases.

  • Enantioselective induction of SIRT1 gene by Syringaresinol from Panax ginseng berry and Acanthopanax senticosus Harms stem.
    Bioorganic & medicinal chemistry letters, 2014
    Co-Authors: Hyun Woo Park, Si Young Cho, Hyun Hee Kim, Bong Sik Yun, Jeong Un Kim, Sang Jun Lee, Jiyong Park
    Abstract:

    Syringaresinol exists either exclusively as one enantiomer or enantiomeric mixtures in plant foods. We found that (+)-Syringaresinol, but not (-)-Syringaresinol, upregulates silent information regulator two ortholog 1 (SIRT1) gene expression, and thus, Panax ginseng berry with predominantly high contents of (+)-Syringaresinol exhibits higher activity in inducing SIRT1 gene expression than Acanthopanax senticosus Harms stem with almost equal proportion of the two enantiomers. These findings highlight the importance of the absolute configuration of Syringaresinol for the biological activity.

Dae Bang Seo - One of the best experts on this subject based on the ideXlab platform.

  • Syringaresinol reverses age related skin atrophy by suppressing foxo3a mediated matrix metalloproteinase 2 activation in copper zinc superoxide dismutase deficient mice
    Journal of Investigative Dermatology, 2019
    Co-Authors: Juewon Kim, Si Young Cho, Toshihiko Toda, Kenji Watanabe, Shuichi Shibuya, Yusuke Ozawa, Naotaka Izuo, Dae Bang Seo, Koutaro Yokote, Takahiko Shimizu
    Abstract:

    Aging is characterized by accumulation of chronic and irreversible oxidative damage, chronic inflammation, and organ dysfunction. Superoxide dismutase (SOD) serves as a major enzyme for cellular superoxide radical metabolism and physiologically regulates cellular redox balance throughout the body. Copper/zinc superoxide dismutase–deficient (SOD1–/–) mice showed diverse phenotypes associated with enhanced oxidative damage in whole organs. Here, we found that oral treatment with Syringaresinol (also known as lirioresinol B), which is the active component in the berries of Korean ginseng (Panax ginseng C.A. Meyer), attenuated the age-related changes in Sod1–/– skin. Interestingly, Syringaresinol morphologically normalized skin atrophy in Sod1–/– mice and promoted fibroblast outgrowth from Sod1–/– skin in vitro. These protective effects were mediated by the suppression of matrix metalloproteinase-2 overproduction in Sod1–/– skin, but not by increased collagen expression. Syringaresinol also decreased the oxidative damage and the phosphorylation of FoxO3a protein, which was a transcriptional factor of matrix metalloproteinase–2, in Sod1–/– skin. These results strongly suggest that Syringaresinol regulates the FoxO3–matrix metalloproteinase-2 axis in oxidative damaged skin and exhibits beneficial effects on age-related skin involution in Sod1–/– mice.

  • Syringaresinol Reverses Age-Related Skin Atrophy by Suppressing FoxO3a-Mediated Matrix Metalloproteinase–2 Activation in Copper/Zinc Superoxide Dismutase–Deficient Mice
    The Journal of investigative dermatology, 2018
    Co-Authors: Juewon Kim, Si Young Cho, Toshihiko Toda, Kenji Watanabe, Shuichi Shibuya, Yusuke Ozawa, Naotaka Izuo, Dae Bang Seo, Koutaro Yokote, Takahiko Shimizu
    Abstract:

    Aging is characterized by accumulation of chronic and irreversible oxidative damage, chronic inflammation, and organ dysfunction. Superoxide dismutase (SOD) serves as a major enzyme for cellular superoxide radical metabolism and physiologically regulates cellular redox balance throughout the body. Copper/zinc superoxide dismutase–deficient (SOD1–/–) mice showed diverse phenotypes associated with enhanced oxidative damage in whole organs. Here, we found that oral treatment with Syringaresinol (also known as lirioresinol B), which is the active component in the berries of Korean ginseng (Panax ginseng C.A. Meyer), attenuated the age-related changes in Sod1–/– skin. Interestingly, Syringaresinol morphologically normalized skin atrophy in Sod1–/– mice and promoted fibroblast outgrowth from Sod1–/– skin in vitro. These protective effects were mediated by the suppression of matrix metalloproteinase-2 overproduction in Sod1–/– skin, but not by increased collagen expression. Syringaresinol also decreased the oxidative damage and the phosphorylation of FoxO3a protein, which was a transcriptional factor of matrix metalloproteinase–2, in Sod1–/– skin. These results strongly suggest that Syringaresinol regulates the FoxO3–matrix metalloproteinase-2 axis in oxidative damaged skin and exhibits beneficial effects on age-related skin involution in Sod1–/– mice.

  • Effects of Korean ginseng berry on skin antipigmentation and antiaging via FoxO3a activation.
    Journal of ginseng research, 2016
    Co-Authors: Juewon Kim, Si Young Cho, Dae Bang Seo, Takahiko Shimizu, Su Hwan Kim, Donghyun Cho, Sunmi Kim, Chan-woong Park, Jae Youl Cho, Song Seok Shin
    Abstract:

    Abstract Background The ginseng berry has various bioactivities, including antidiabetic, anticancer, antiinflammatory, and antioxidative properties. Moreover, we have revealed that the active antiaging component of the ginseng berry, Syringaresinol, has the ability to stimulate longevity via gene activation. Despite the many known beneficial effects of ginseng, its effects on skin aging are poorly understood. In this study, we investigated the effects of ginseng and the ginseng berry on one of the skin aging processes, melanogenesis, and age-related pigment lipofuscin accumulation, to elucidate the mechanism of action with respect to antiaging. Methods The human melanoma MNT1 cell line was treated with ginseng root extract, ginseng berry extract, or Syringaresinol. Then, the cells were analyzed using a melanin assay, and the tyrosinase activity was estimated. The Caenorhabditis elegans wild type N2 strain was used for the life span assay to analyze the antiaging effects of the samples. A lipofuscin fluorescence assay was performed during 10 passages with the Syringaresinol treatment. Results A 7-d treatment with ginseng berry extract reduced melanin accumulation and tyrosinase activity more than ginseng root extract. These results may be due to the active compound of the ginseng berry, Syringaresinol. The antimelanogenic activity was strongly coordinated with the activation of the longevity gene foxo3a . Moreover, the ginseng berry extract had more potent antiaging effects, caused a life span extension, and reduced lipofuscin accumulation. Conclusion Taken together, our results suggest that these antimelanogenic effects and antiaging effects of ginseng berry mediate the activation of antioxidation–FoxO3a signaling.

  • Identification of a small molecule activator of SIRT1 gene expression.
    Aging, 2013
    Co-Authors: Si Young Cho, Sang Jun Lee, Dae Bang Seo, Miook Cho, Yousin Suh
    Abstract:

    Increased SIRT1 expression exerts beneficial effects in transgenic animal models, ameliorating the onset and progression of aging-related disease phenotypes in various organs including the heart. The potential beneficial effects of SIRT1 have made SIRT1 a prime therapeutic target for age-related diseases and considerable efforts led to the identification of small molecule activator of SIRT1 protein. Thus far, however, a small molecule activator of SIRT1 gene expression has not been reported. Here, we report that Syringaresinol, isolated from Panax ginseng berry pulp, is an activator of SIRT1 gene expression. Using human umbilical endothelial cells (HUVECs), we show that Syringaresinol treatment induced binding of FOXO3 to the SIRT1 promoter in a sequence-specific manner, leading to induction of SIRT1 expression. Increased SIRT1 expression in HUVECs by Syringaresinol treatment delayed cellular senescence and improved various markers of endothelial functions in a FOXO3 dependent manner. Collectively, these findings bring to light a new transcription activator of SIRT1 that may have therapeutic potential.

Koutaro Yokote - One of the best experts on this subject based on the ideXlab platform.

  • Syringaresinol reverses age related skin atrophy by suppressing foxo3a mediated matrix metalloproteinase 2 activation in copper zinc superoxide dismutase deficient mice
    Journal of Investigative Dermatology, 2019
    Co-Authors: Juewon Kim, Si Young Cho, Toshihiko Toda, Kenji Watanabe, Shuichi Shibuya, Yusuke Ozawa, Naotaka Izuo, Dae Bang Seo, Koutaro Yokote, Takahiko Shimizu
    Abstract:

    Aging is characterized by accumulation of chronic and irreversible oxidative damage, chronic inflammation, and organ dysfunction. Superoxide dismutase (SOD) serves as a major enzyme for cellular superoxide radical metabolism and physiologically regulates cellular redox balance throughout the body. Copper/zinc superoxide dismutase–deficient (SOD1–/–) mice showed diverse phenotypes associated with enhanced oxidative damage in whole organs. Here, we found that oral treatment with Syringaresinol (also known as lirioresinol B), which is the active component in the berries of Korean ginseng (Panax ginseng C.A. Meyer), attenuated the age-related changes in Sod1–/– skin. Interestingly, Syringaresinol morphologically normalized skin atrophy in Sod1–/– mice and promoted fibroblast outgrowth from Sod1–/– skin in vitro. These protective effects were mediated by the suppression of matrix metalloproteinase-2 overproduction in Sod1–/– skin, but not by increased collagen expression. Syringaresinol also decreased the oxidative damage and the phosphorylation of FoxO3a protein, which was a transcriptional factor of matrix metalloproteinase–2, in Sod1–/– skin. These results strongly suggest that Syringaresinol regulates the FoxO3–matrix metalloproteinase-2 axis in oxidative damaged skin and exhibits beneficial effects on age-related skin involution in Sod1–/– mice.

  • Syringaresinol Reverses Age-Related Skin Atrophy by Suppressing FoxO3a-Mediated Matrix Metalloproteinase–2 Activation in Copper/Zinc Superoxide Dismutase–Deficient Mice
    The Journal of investigative dermatology, 2018
    Co-Authors: Juewon Kim, Si Young Cho, Toshihiko Toda, Kenji Watanabe, Shuichi Shibuya, Yusuke Ozawa, Naotaka Izuo, Dae Bang Seo, Koutaro Yokote, Takahiko Shimizu
    Abstract:

    Aging is characterized by accumulation of chronic and irreversible oxidative damage, chronic inflammation, and organ dysfunction. Superoxide dismutase (SOD) serves as a major enzyme for cellular superoxide radical metabolism and physiologically regulates cellular redox balance throughout the body. Copper/zinc superoxide dismutase–deficient (SOD1–/–) mice showed diverse phenotypes associated with enhanced oxidative damage in whole organs. Here, we found that oral treatment with Syringaresinol (also known as lirioresinol B), which is the active component in the berries of Korean ginseng (Panax ginseng C.A. Meyer), attenuated the age-related changes in Sod1–/– skin. Interestingly, Syringaresinol morphologically normalized skin atrophy in Sod1–/– mice and promoted fibroblast outgrowth from Sod1–/– skin in vitro. These protective effects were mediated by the suppression of matrix metalloproteinase-2 overproduction in Sod1–/– skin, but not by increased collagen expression. Syringaresinol also decreased the oxidative damage and the phosphorylation of FoxO3a protein, which was a transcriptional factor of matrix metalloproteinase–2, in Sod1–/– skin. These results strongly suggest that Syringaresinol regulates the FoxO3–matrix metalloproteinase-2 axis in oxidative damaged skin and exhibits beneficial effects on age-related skin involution in Sod1–/– mice.