author_facet Yu, Weihua
Zhang, Xiaodi
Wu, Hao
Zhou, Qingbiao
Wang, Zhao
Liu, Rui
Liu, Jiangzheng
Wang, Xin
Hai, Chunxu
Yu, Weihua
Zhang, Xiaodi
Wu, Hao
Zhou, Qingbiao
Wang, Zhao
Liu, Rui
Liu, Jiangzheng
Wang, Xin
Hai, Chunxu
author Yu, Weihua
Zhang, Xiaodi
Wu, Hao
Zhou, Qingbiao
Wang, Zhao
Liu, Rui
Liu, Jiangzheng
Wang, Xin
Hai, Chunxu
spellingShingle Yu, Weihua
Zhang, Xiaodi
Wu, Hao
Zhou, Qingbiao
Wang, Zhao
Liu, Rui
Liu, Jiangzheng
Wang, Xin
Hai, Chunxu
Oxidative Medicine and Cellular Longevity
HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
Cell Biology
Aging
General Medicine
Biochemistry
author_sort yu, weihua
spelling Yu, Weihua Zhang, Xiaodi Wu, Hao Zhou, Qingbiao Wang, Zhao Liu, Rui Liu, Jiangzheng Wang, Xin Hai, Chunxu 1942-0900 1942-0994 Hindawi Limited Cell Biology Aging General Medicine Biochemistry http://dx.doi.org/10.1155/2017/1818575 <jats:p>2,3,5,4′-Tetrahydroxystilbene-2-O-<jats:italic>β</jats:italic>-D-glucoside (TSG), an important monomer extracted from Polygonum multiflorum, can prevent a number of inflammation associated chronic diseases. However, the mechanism involved in TSG inducing anti-inflammatory role remains unclear. As an inducible antioxidant enzyme, Heme oxygenase-1 (HO-1), is crucial for protecting the mammalian cells against adverse stimuli. Here, we found that the TSG treatment strongly induces the expression of HO-1 in an NRF2-depended manner. Meanwhile, TSG increased the mitochondrial mass through upregulation of the mitochondrial biogenesis activators (PGC-1<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi>α</mml:mi></mml:mrow></mml:math>, NRF1, and TFAM) as well as the mitochondrial complex IV. Furthermore, TSG attenuated Lipopolysaccharide (LPS) mediated RAW264.7 cells activation and secretion of proinflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-<jats:italic>α</jats:italic> (TNF-<jats:italic>α</jats:italic>). Zinc Protoporphyrin (ZnPP), a selective inhibitor of HO-1 activity, was able to attenuate TSG mediated mitochondrial biogenesis and anti-inflammatory process. Finally, we observed that LPS induced obvious mtDNA depletion and ATP deficiency, which indicated a severe damage of mitochondria. TSG restored the LPS induced mitochondrial dysfunction via activation of the mitochondrial biogenesis. ZnPP treatment markedly reversed the inhibitory effects of TSG on mitochondrial damage and oxidative stress in LPS stimulated macrophages. Taken together, these findings suggest that TSG enhances mitochondrial biogenesis and function mainly via activation the HO-1. TSG can be developed as a potential drug for treatment of inflammatory diseases.</jats:p> HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages Oxidative Medicine and Cellular Longevity
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series Oxidative Medicine and Cellular Longevity
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title HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
title_unstemmed HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
title_full HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
title_fullStr HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
title_full_unstemmed HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
title_short HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
title_sort ho-1 is essential for tetrahydroxystilbene glucoside mediated mitochondrial biogenesis and anti-inflammation process in lps-treated raw264.7 macrophages
topic Cell Biology
Aging
General Medicine
Biochemistry
url http://dx.doi.org/10.1155/2017/1818575
publishDate 2017
physical 1-13
description <jats:p>2,3,5,4′-Tetrahydroxystilbene-2-O-<jats:italic>β</jats:italic>-D-glucoside (TSG), an important monomer extracted from Polygonum multiflorum, can prevent a number of inflammation associated chronic diseases. However, the mechanism involved in TSG inducing anti-inflammatory role remains unclear. As an inducible antioxidant enzyme, Heme oxygenase-1 (HO-1), is crucial for protecting the mammalian cells against adverse stimuli. Here, we found that the TSG treatment strongly induces the expression of HO-1 in an NRF2-depended manner. Meanwhile, TSG increased the mitochondrial mass through upregulation of the mitochondrial biogenesis activators (PGC-1<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi>α</mml:mi></mml:mrow></mml:math>, NRF1, and TFAM) as well as the mitochondrial complex IV. Furthermore, TSG attenuated Lipopolysaccharide (LPS) mediated RAW264.7 cells activation and secretion of proinflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-<jats:italic>α</jats:italic> (TNF-<jats:italic>α</jats:italic>). Zinc Protoporphyrin (ZnPP), a selective inhibitor of HO-1 activity, was able to attenuate TSG mediated mitochondrial biogenesis and anti-inflammatory process. Finally, we observed that LPS induced obvious mtDNA depletion and ATP deficiency, which indicated a severe damage of mitochondria. TSG restored the LPS induced mitochondrial dysfunction via activation of the mitochondrial biogenesis. ZnPP treatment markedly reversed the inhibitory effects of TSG on mitochondrial damage and oxidative stress in LPS stimulated macrophages. Taken together, these findings suggest that TSG enhances mitochondrial biogenesis and function mainly via activation the HO-1. TSG can be developed as a potential drug for treatment of inflammatory diseases.</jats:p>
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author Yu, Weihua, Zhang, Xiaodi, Wu, Hao, Zhou, Qingbiao, Wang, Zhao, Liu, Rui, Liu, Jiangzheng, Wang, Xin, Hai, Chunxu
author_facet Yu, Weihua, Zhang, Xiaodi, Wu, Hao, Zhou, Qingbiao, Wang, Zhao, Liu, Rui, Liu, Jiangzheng, Wang, Xin, Hai, Chunxu, Yu, Weihua, Zhang, Xiaodi, Wu, Hao, Zhou, Qingbiao, Wang, Zhao, Liu, Rui, Liu, Jiangzheng, Wang, Xin, Hai, Chunxu
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description <jats:p>2,3,5,4′-Tetrahydroxystilbene-2-O-<jats:italic>β</jats:italic>-D-glucoside (TSG), an important monomer extracted from Polygonum multiflorum, can prevent a number of inflammation associated chronic diseases. However, the mechanism involved in TSG inducing anti-inflammatory role remains unclear. As an inducible antioxidant enzyme, Heme oxygenase-1 (HO-1), is crucial for protecting the mammalian cells against adverse stimuli. Here, we found that the TSG treatment strongly induces the expression of HO-1 in an NRF2-depended manner. Meanwhile, TSG increased the mitochondrial mass through upregulation of the mitochondrial biogenesis activators (PGC-1<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi>α</mml:mi></mml:mrow></mml:math>, NRF1, and TFAM) as well as the mitochondrial complex IV. Furthermore, TSG attenuated Lipopolysaccharide (LPS) mediated RAW264.7 cells activation and secretion of proinflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-<jats:italic>α</jats:italic> (TNF-<jats:italic>α</jats:italic>). Zinc Protoporphyrin (ZnPP), a selective inhibitor of HO-1 activity, was able to attenuate TSG mediated mitochondrial biogenesis and anti-inflammatory process. Finally, we observed that LPS induced obvious mtDNA depletion and ATP deficiency, which indicated a severe damage of mitochondria. TSG restored the LPS induced mitochondrial dysfunction via activation of the mitochondrial biogenesis. ZnPP treatment markedly reversed the inhibitory effects of TSG on mitochondrial damage and oxidative stress in LPS stimulated macrophages. Taken together, these findings suggest that TSG enhances mitochondrial biogenesis and function mainly via activation the HO-1. TSG can be developed as a potential drug for treatment of inflammatory diseases.</jats:p>
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spelling Yu, Weihua Zhang, Xiaodi Wu, Hao Zhou, Qingbiao Wang, Zhao Liu, Rui Liu, Jiangzheng Wang, Xin Hai, Chunxu 1942-0900 1942-0994 Hindawi Limited Cell Biology Aging General Medicine Biochemistry http://dx.doi.org/10.1155/2017/1818575 <jats:p>2,3,5,4′-Tetrahydroxystilbene-2-O-<jats:italic>β</jats:italic>-D-glucoside (TSG), an important monomer extracted from Polygonum multiflorum, can prevent a number of inflammation associated chronic diseases. However, the mechanism involved in TSG inducing anti-inflammatory role remains unclear. As an inducible antioxidant enzyme, Heme oxygenase-1 (HO-1), is crucial for protecting the mammalian cells against adverse stimuli. Here, we found that the TSG treatment strongly induces the expression of HO-1 in an NRF2-depended manner. Meanwhile, TSG increased the mitochondrial mass through upregulation of the mitochondrial biogenesis activators (PGC-1<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi>α</mml:mi></mml:mrow></mml:math>, NRF1, and TFAM) as well as the mitochondrial complex IV. Furthermore, TSG attenuated Lipopolysaccharide (LPS) mediated RAW264.7 cells activation and secretion of proinflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-<jats:italic>α</jats:italic> (TNF-<jats:italic>α</jats:italic>). Zinc Protoporphyrin (ZnPP), a selective inhibitor of HO-1 activity, was able to attenuate TSG mediated mitochondrial biogenesis and anti-inflammatory process. Finally, we observed that LPS induced obvious mtDNA depletion and ATP deficiency, which indicated a severe damage of mitochondria. TSG restored the LPS induced mitochondrial dysfunction via activation of the mitochondrial biogenesis. ZnPP treatment markedly reversed the inhibitory effects of TSG on mitochondrial damage and oxidative stress in LPS stimulated macrophages. Taken together, these findings suggest that TSG enhances mitochondrial biogenesis and function mainly via activation the HO-1. TSG can be developed as a potential drug for treatment of inflammatory diseases.</jats:p> HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages Oxidative Medicine and Cellular Longevity
spellingShingle Yu, Weihua, Zhang, Xiaodi, Wu, Hao, Zhou, Qingbiao, Wang, Zhao, Liu, Rui, Liu, Jiangzheng, Wang, Xin, Hai, Chunxu, Oxidative Medicine and Cellular Longevity, HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages, Cell Biology, Aging, General Medicine, Biochemistry
title HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
title_full HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
title_fullStr HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
title_full_unstemmed HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
title_short HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
title_sort ho-1 is essential for tetrahydroxystilbene glucoside mediated mitochondrial biogenesis and anti-inflammation process in lps-treated raw264.7 macrophages
title_unstemmed HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages
topic Cell Biology, Aging, General Medicine, Biochemistry
url http://dx.doi.org/10.1155/2017/1818575