Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects

Postmenopausal osteoporosis (PMOP) is a common bone disease characterized by decreased bone density and increased bone fragility due to decreased estrogen levels. Qiangguyin (QGY) is transformed from the famous traditional Chinese medicine BuShen Invigorating Blood Decoction. In this study, we used...
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Autor*in:	Jingyuan Wen [verfasserIn] Zhengsheng Bao [verfasserIn] Lunxin Li [verfasserIn] Yingquan Liu [verfasserIn] Bing Wei [verfasserIn] Xiaoang Ye [verfasserIn] Huihui Xu [verfasserIn] Longkang Cui [verfasserIn] Xuefei Li [verfasserIn] Gaobo Shen [verfasserIn] Yuan Fang [verfasserIn] Hanbing Zeng [verfasserIn] Zhe Shen [verfasserIn] Enping Guo [verfasserIn] Hongting Jin [verfasserIn] Lianguo Wu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Qiangguyin P38 MAPK Postmenopausal osteoporosis Lipid differentiation Chondro-osseous junction

Übergeordnetes Werk:	In: Biomedicine & Pharmacotherapy - Elsevier, 2021, 158(2023), Seite 114122-
Übergeordnetes Werk:	volume:158 ; year:2023 ; pages:114122-

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.biopha.2022.114122

Katalog-ID:	DOAJ020802072

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520			\|a Postmenopausal osteoporosis (PMOP) is a common bone disease characterized by decreased bone density and increased bone fragility due to decreased estrogen levels. Qiangguyin (QGY) is transformed from the famous traditional Chinese medicine BuShen Invigorating Blood Decoction. In this study, we used QGY to treat PMOP. We observed that QGY significantly reduced fat accumulation in the chondro-osseous junction. However, its specific mechanism of action remains unclear. To determine the specific molecular mechanism of QGY, we explored the pharmacological mechanism by which QGY reduces fat accumulation in the chondro-osseous junction through network pharmacological analysis. The active components and targets related to PMOP and QGY were screened from different databases, forming a composition-target-disease network. Next, a comprehensive analysis platform including protein-protein interaction (PPI) network, Gene Ontology (GO) enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were established. The results revealed that QGY inhibits adipogenic differentiation by activating the mitogen-activated protein kinase (MAPK) signaling pathway, thus reducing the accumulation of fat in the chondro-osseous junction. For further verification. In vitro and in vivo experiments were carried out. Our data showed that QGY significantly reversed the high expression of fatty acid binding protein 4 (FABP4) and peroxisome proliferator-activated receptor γ (PPARγ). Further, QGY prevents fat accumulation by inhibiting the expression of p38. In summary, the results of this study suggested that QGY-induced phenotypic changes are related to the activation of the p38 MAPK signaling pathway.
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allfields	10.1016/j.biopha.2022.114122 doi (DE-627)DOAJ020802072 (DE-599)DOAJ593b8e809b0949448b0a4e9fb024cbef DE-627 ger DE-627 rakwb eng RM1-950 Jingyuan Wen verfasserin aut Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Postmenopausal osteoporosis (PMOP) is a common bone disease characterized by decreased bone density and increased bone fragility due to decreased estrogen levels. Qiangguyin (QGY) is transformed from the famous traditional Chinese medicine BuShen Invigorating Blood Decoction. In this study, we used QGY to treat PMOP. We observed that QGY significantly reduced fat accumulation in the chondro-osseous junction. However, its specific mechanism of action remains unclear. To determine the specific molecular mechanism of QGY, we explored the pharmacological mechanism by which QGY reduces fat accumulation in the chondro-osseous junction through network pharmacological analysis. The active components and targets related to PMOP and QGY were screened from different databases, forming a composition-target-disease network. Next, a comprehensive analysis platform including protein-protein interaction (PPI) network, Gene Ontology (GO) enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were established. The results revealed that QGY inhibits adipogenic differentiation by activating the mitogen-activated protein kinase (MAPK) signaling pathway, thus reducing the accumulation of fat in the chondro-osseous junction. For further verification. In vitro and in vivo experiments were carried out. Our data showed that QGY significantly reversed the high expression of fatty acid binding protein 4 (FABP4) and peroxisome proliferator-activated receptor γ (PPARγ). Further, QGY prevents fat accumulation by inhibiting the expression of p38. In summary, the results of this study suggested that QGY-induced phenotypic changes are related to the activation of the p38 MAPK signaling pathway. Qiangguyin P38 MAPK Postmenopausal osteoporosis Lipid differentiation Chondro-osseous junction Therapeutics. Pharmacology Zhengsheng Bao verfasserin aut Lunxin Li verfasserin aut Yingquan Liu verfasserin aut Bing Wei verfasserin aut Xiaoang Ye verfasserin aut Huihui Xu verfasserin aut Longkang Cui verfasserin aut Xuefei Li verfasserin aut Gaobo Shen verfasserin aut Yuan Fang verfasserin aut Hanbing Zeng verfasserin aut Zhe Shen verfasserin aut Enping Guo verfasserin aut Hongting Jin verfasserin aut Lianguo Wu verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 158(2023), Seite 114122- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:158 year:2023 pages:114122- https://doi.org/10.1016/j.biopha.2022.114122 kostenfrei https://doaj.org/article/593b8e809b0949448b0a4e9fb024cbef kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332222015116 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 158 2023 114122-
spelling	10.1016/j.biopha.2022.114122 doi (DE-627)DOAJ020802072 (DE-599)DOAJ593b8e809b0949448b0a4e9fb024cbef DE-627 ger DE-627 rakwb eng RM1-950 Jingyuan Wen verfasserin aut Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Postmenopausal osteoporosis (PMOP) is a common bone disease characterized by decreased bone density and increased bone fragility due to decreased estrogen levels. Qiangguyin (QGY) is transformed from the famous traditional Chinese medicine BuShen Invigorating Blood Decoction. In this study, we used QGY to treat PMOP. We observed that QGY significantly reduced fat accumulation in the chondro-osseous junction. However, its specific mechanism of action remains unclear. To determine the specific molecular mechanism of QGY, we explored the pharmacological mechanism by which QGY reduces fat accumulation in the chondro-osseous junction through network pharmacological analysis. The active components and targets related to PMOP and QGY were screened from different databases, forming a composition-target-disease network. Next, a comprehensive analysis platform including protein-protein interaction (PPI) network, Gene Ontology (GO) enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were established. The results revealed that QGY inhibits adipogenic differentiation by activating the mitogen-activated protein kinase (MAPK) signaling pathway, thus reducing the accumulation of fat in the chondro-osseous junction. For further verification. In vitro and in vivo experiments were carried out. Our data showed that QGY significantly reversed the high expression of fatty acid binding protein 4 (FABP4) and peroxisome proliferator-activated receptor γ (PPARγ). Further, QGY prevents fat accumulation by inhibiting the expression of p38. In summary, the results of this study suggested that QGY-induced phenotypic changes are related to the activation of the p38 MAPK signaling pathway. Qiangguyin P38 MAPK Postmenopausal osteoporosis Lipid differentiation Chondro-osseous junction Therapeutics. Pharmacology Zhengsheng Bao verfasserin aut Lunxin Li verfasserin aut Yingquan Liu verfasserin aut Bing Wei verfasserin aut Xiaoang Ye verfasserin aut Huihui Xu verfasserin aut Longkang Cui verfasserin aut Xuefei Li verfasserin aut Gaobo Shen verfasserin aut Yuan Fang verfasserin aut Hanbing Zeng verfasserin aut Zhe Shen verfasserin aut Enping Guo verfasserin aut Hongting Jin verfasserin aut Lianguo Wu verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 158(2023), Seite 114122- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:158 year:2023 pages:114122- https://doi.org/10.1016/j.biopha.2022.114122 kostenfrei https://doaj.org/article/593b8e809b0949448b0a4e9fb024cbef kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332222015116 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 158 2023 114122-
allfields_unstemmed	10.1016/j.biopha.2022.114122 doi (DE-627)DOAJ020802072 (DE-599)DOAJ593b8e809b0949448b0a4e9fb024cbef DE-627 ger DE-627 rakwb eng RM1-950 Jingyuan Wen verfasserin aut Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Postmenopausal osteoporosis (PMOP) is a common bone disease characterized by decreased bone density and increased bone fragility due to decreased estrogen levels. Qiangguyin (QGY) is transformed from the famous traditional Chinese medicine BuShen Invigorating Blood Decoction. In this study, we used QGY to treat PMOP. We observed that QGY significantly reduced fat accumulation in the chondro-osseous junction. However, its specific mechanism of action remains unclear. To determine the specific molecular mechanism of QGY, we explored the pharmacological mechanism by which QGY reduces fat accumulation in the chondro-osseous junction through network pharmacological analysis. The active components and targets related to PMOP and QGY were screened from different databases, forming a composition-target-disease network. Next, a comprehensive analysis platform including protein-protein interaction (PPI) network, Gene Ontology (GO) enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were established. The results revealed that QGY inhibits adipogenic differentiation by activating the mitogen-activated protein kinase (MAPK) signaling pathway, thus reducing the accumulation of fat in the chondro-osseous junction. For further verification. In vitro and in vivo experiments were carried out. Our data showed that QGY significantly reversed the high expression of fatty acid binding protein 4 (FABP4) and peroxisome proliferator-activated receptor γ (PPARγ). Further, QGY prevents fat accumulation by inhibiting the expression of p38. In summary, the results of this study suggested that QGY-induced phenotypic changes are related to the activation of the p38 MAPK signaling pathway. Qiangguyin P38 MAPK Postmenopausal osteoporosis Lipid differentiation Chondro-osseous junction Therapeutics. Pharmacology Zhengsheng Bao verfasserin aut Lunxin Li verfasserin aut Yingquan Liu verfasserin aut Bing Wei verfasserin aut Xiaoang Ye verfasserin aut Huihui Xu verfasserin aut Longkang Cui verfasserin aut Xuefei Li verfasserin aut Gaobo Shen verfasserin aut Yuan Fang verfasserin aut Hanbing Zeng verfasserin aut Zhe Shen verfasserin aut Enping Guo verfasserin aut Hongting Jin verfasserin aut Lianguo Wu verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 158(2023), Seite 114122- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:158 year:2023 pages:114122- https://doi.org/10.1016/j.biopha.2022.114122 kostenfrei https://doaj.org/article/593b8e809b0949448b0a4e9fb024cbef kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332222015116 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 158 2023 114122-
allfieldsGer	10.1016/j.biopha.2022.114122 doi (DE-627)DOAJ020802072 (DE-599)DOAJ593b8e809b0949448b0a4e9fb024cbef DE-627 ger DE-627 rakwb eng RM1-950 Jingyuan Wen verfasserin aut Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Postmenopausal osteoporosis (PMOP) is a common bone disease characterized by decreased bone density and increased bone fragility due to decreased estrogen levels. Qiangguyin (QGY) is transformed from the famous traditional Chinese medicine BuShen Invigorating Blood Decoction. In this study, we used QGY to treat PMOP. We observed that QGY significantly reduced fat accumulation in the chondro-osseous junction. However, its specific mechanism of action remains unclear. To determine the specific molecular mechanism of QGY, we explored the pharmacological mechanism by which QGY reduces fat accumulation in the chondro-osseous junction through network pharmacological analysis. The active components and targets related to PMOP and QGY were screened from different databases, forming a composition-target-disease network. Next, a comprehensive analysis platform including protein-protein interaction (PPI) network, Gene Ontology (GO) enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were established. The results revealed that QGY inhibits adipogenic differentiation by activating the mitogen-activated protein kinase (MAPK) signaling pathway, thus reducing the accumulation of fat in the chondro-osseous junction. For further verification. In vitro and in vivo experiments were carried out. Our data showed that QGY significantly reversed the high expression of fatty acid binding protein 4 (FABP4) and peroxisome proliferator-activated receptor γ (PPARγ). Further, QGY prevents fat accumulation by inhibiting the expression of p38. In summary, the results of this study suggested that QGY-induced phenotypic changes are related to the activation of the p38 MAPK signaling pathway. Qiangguyin P38 MAPK Postmenopausal osteoporosis Lipid differentiation Chondro-osseous junction Therapeutics. Pharmacology Zhengsheng Bao verfasserin aut Lunxin Li verfasserin aut Yingquan Liu verfasserin aut Bing Wei verfasserin aut Xiaoang Ye verfasserin aut Huihui Xu verfasserin aut Longkang Cui verfasserin aut Xuefei Li verfasserin aut Gaobo Shen verfasserin aut Yuan Fang verfasserin aut Hanbing Zeng verfasserin aut Zhe Shen verfasserin aut Enping Guo verfasserin aut Hongting Jin verfasserin aut Lianguo Wu verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 158(2023), Seite 114122- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:158 year:2023 pages:114122- https://doi.org/10.1016/j.biopha.2022.114122 kostenfrei https://doaj.org/article/593b8e809b0949448b0a4e9fb024cbef kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332222015116 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 158 2023 114122-
allfieldsSound	10.1016/j.biopha.2022.114122 doi (DE-627)DOAJ020802072 (DE-599)DOAJ593b8e809b0949448b0a4e9fb024cbef DE-627 ger DE-627 rakwb eng RM1-950 Jingyuan Wen verfasserin aut Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Postmenopausal osteoporosis (PMOP) is a common bone disease characterized by decreased bone density and increased bone fragility due to decreased estrogen levels. Qiangguyin (QGY) is transformed from the famous traditional Chinese medicine BuShen Invigorating Blood Decoction. In this study, we used QGY to treat PMOP. We observed that QGY significantly reduced fat accumulation in the chondro-osseous junction. However, its specific mechanism of action remains unclear. To determine the specific molecular mechanism of QGY, we explored the pharmacological mechanism by which QGY reduces fat accumulation in the chondro-osseous junction through network pharmacological analysis. The active components and targets related to PMOP and QGY were screened from different databases, forming a composition-target-disease network. Next, a comprehensive analysis platform including protein-protein interaction (PPI) network, Gene Ontology (GO) enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were established. The results revealed that QGY inhibits adipogenic differentiation by activating the mitogen-activated protein kinase (MAPK) signaling pathway, thus reducing the accumulation of fat in the chondro-osseous junction. For further verification. In vitro and in vivo experiments were carried out. Our data showed that QGY significantly reversed the high expression of fatty acid binding protein 4 (FABP4) and peroxisome proliferator-activated receptor γ (PPARγ). Further, QGY prevents fat accumulation by inhibiting the expression of p38. In summary, the results of this study suggested that QGY-induced phenotypic changes are related to the activation of the p38 MAPK signaling pathway. Qiangguyin P38 MAPK Postmenopausal osteoporosis Lipid differentiation Chondro-osseous junction Therapeutics. Pharmacology Zhengsheng Bao verfasserin aut Lunxin Li verfasserin aut Yingquan Liu verfasserin aut Bing Wei verfasserin aut Xiaoang Ye verfasserin aut Huihui Xu verfasserin aut Longkang Cui verfasserin aut Xuefei Li verfasserin aut Gaobo Shen verfasserin aut Yuan Fang verfasserin aut Hanbing Zeng verfasserin aut Zhe Shen verfasserin aut Enping Guo verfasserin aut Hongting Jin verfasserin aut Lianguo Wu verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 158(2023), Seite 114122- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:158 year:2023 pages:114122- https://doi.org/10.1016/j.biopha.2022.114122 kostenfrei https://doaj.org/article/593b8e809b0949448b0a4e9fb024cbef kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332222015116 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 158 2023 114122-
language	English
source	In Biomedicine & Pharmacotherapy 158(2023), Seite 114122- volume:158 year:2023 pages:114122-
sourceStr	In Biomedicine & Pharmacotherapy 158(2023), Seite 114122- volume:158 year:2023 pages:114122-
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Qiangguyin P38 MAPK Postmenopausal osteoporosis Lipid differentiation Chondro-osseous junction Therapeutics. Pharmacology
isfreeaccess_bool	true
container_title	Biomedicine & Pharmacotherapy
authorswithroles_txt_mv	Jingyuan Wen @@aut@@ Zhengsheng Bao @@aut@@ Lunxin Li @@aut@@ Yingquan Liu @@aut@@ Bing Wei @@aut@@ Xiaoang Ye @@aut@@ Huihui Xu @@aut@@ Longkang Cui @@aut@@ Xuefei Li @@aut@@ Gaobo Shen @@aut@@ Yuan Fang @@aut@@ Hanbing Zeng @@aut@@ Zhe Shen @@aut@@ Enping Guo @@aut@@ Hongting Jin @@aut@@ Lianguo Wu @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
hierarchy_top_id	306717565
id	DOAJ020802072
language_de	englisch
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callnumber-first	R - Medicine
author	Jingyuan Wen
spellingShingle	Jingyuan Wen misc RM1-950 misc Qiangguyin misc P38 MAPK misc Postmenopausal osteoporosis misc Lipid differentiation misc Chondro-osseous junction misc Therapeutics. Pharmacology Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects
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topic_title	RM1-950 Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects Qiangguyin P38 MAPK Postmenopausal osteoporosis Lipid differentiation Chondro-osseous junction
topic	misc RM1-950 misc Qiangguyin misc P38 MAPK misc Postmenopausal osteoporosis misc Lipid differentiation misc Chondro-osseous junction misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc Qiangguyin misc P38 MAPK misc Postmenopausal osteoporosis misc Lipid differentiation misc Chondro-osseous junction misc Therapeutics. Pharmacology
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title	Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects
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title_full	Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects
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author_browse	Jingyuan Wen Zhengsheng Bao Lunxin Li Yingquan Liu Bing Wei Xiaoang Ye Huihui Xu Longkang Cui Xuefei Li Gaobo Shen Yuan Fang Hanbing Zeng Zhe Shen Enping Guo Hongting Jin Lianguo Wu
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title_sort	qiangguyin inhibited fat accumulation in ovx mice through the p38 mapk signaling pathway to achieve anti-osteoporosis effects
callnumber	RM1-950
title_auth	Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects
abstract	Postmenopausal osteoporosis (PMOP) is a common bone disease characterized by decreased bone density and increased bone fragility due to decreased estrogen levels. Qiangguyin (QGY) is transformed from the famous traditional Chinese medicine BuShen Invigorating Blood Decoction. In this study, we used QGY to treat PMOP. We observed that QGY significantly reduced fat accumulation in the chondro-osseous junction. However, its specific mechanism of action remains unclear. To determine the specific molecular mechanism of QGY, we explored the pharmacological mechanism by which QGY reduces fat accumulation in the chondro-osseous junction through network pharmacological analysis. The active components and targets related to PMOP and QGY were screened from different databases, forming a composition-target-disease network. Next, a comprehensive analysis platform including protein-protein interaction (PPI) network, Gene Ontology (GO) enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were established. The results revealed that QGY inhibits adipogenic differentiation by activating the mitogen-activated protein kinase (MAPK) signaling pathway, thus reducing the accumulation of fat in the chondro-osseous junction. For further verification. In vitro and in vivo experiments were carried out. Our data showed that QGY significantly reversed the high expression of fatty acid binding protein 4 (FABP4) and peroxisome proliferator-activated receptor γ (PPARγ). Further, QGY prevents fat accumulation by inhibiting the expression of p38. In summary, the results of this study suggested that QGY-induced phenotypic changes are related to the activation of the p38 MAPK signaling pathway.
abstractGer	Postmenopausal osteoporosis (PMOP) is a common bone disease characterized by decreased bone density and increased bone fragility due to decreased estrogen levels. Qiangguyin (QGY) is transformed from the famous traditional Chinese medicine BuShen Invigorating Blood Decoction. In this study, we used QGY to treat PMOP. We observed that QGY significantly reduced fat accumulation in the chondro-osseous junction. However, its specific mechanism of action remains unclear. To determine the specific molecular mechanism of QGY, we explored the pharmacological mechanism by which QGY reduces fat accumulation in the chondro-osseous junction through network pharmacological analysis. The active components and targets related to PMOP and QGY were screened from different databases, forming a composition-target-disease network. Next, a comprehensive analysis platform including protein-protein interaction (PPI) network, Gene Ontology (GO) enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were established. The results revealed that QGY inhibits adipogenic differentiation by activating the mitogen-activated protein kinase (MAPK) signaling pathway, thus reducing the accumulation of fat in the chondro-osseous junction. For further verification. In vitro and in vivo experiments were carried out. Our data showed that QGY significantly reversed the high expression of fatty acid binding protein 4 (FABP4) and peroxisome proliferator-activated receptor γ (PPARγ). Further, QGY prevents fat accumulation by inhibiting the expression of p38. In summary, the results of this study suggested that QGY-induced phenotypic changes are related to the activation of the p38 MAPK signaling pathway.
abstract_unstemmed	Postmenopausal osteoporosis (PMOP) is a common bone disease characterized by decreased bone density and increased bone fragility due to decreased estrogen levels. Qiangguyin (QGY) is transformed from the famous traditional Chinese medicine BuShen Invigorating Blood Decoction. In this study, we used QGY to treat PMOP. We observed that QGY significantly reduced fat accumulation in the chondro-osseous junction. However, its specific mechanism of action remains unclear. To determine the specific molecular mechanism of QGY, we explored the pharmacological mechanism by which QGY reduces fat accumulation in the chondro-osseous junction through network pharmacological analysis. The active components and targets related to PMOP and QGY were screened from different databases, forming a composition-target-disease network. Next, a comprehensive analysis platform including protein-protein interaction (PPI) network, Gene Ontology (GO) enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were established. The results revealed that QGY inhibits adipogenic differentiation by activating the mitogen-activated protein kinase (MAPK) signaling pathway, thus reducing the accumulation of fat in the chondro-osseous junction. For further verification. In vitro and in vivo experiments were carried out. Our data showed that QGY significantly reversed the high expression of fatty acid binding protein 4 (FABP4) and peroxisome proliferator-activated receptor γ (PPARγ). Further, QGY prevents fat accumulation by inhibiting the expression of p38. In summary, the results of this study suggested that QGY-induced phenotypic changes are related to the activation of the p38 MAPK signaling pathway.
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title_short	Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects
url	https://doi.org/10.1016/j.biopha.2022.114122 https://doaj.org/article/593b8e809b0949448b0a4e9fb024cbef http://www.sciencedirect.com/science/article/pii/S0753332222015116 https://doaj.org/toc/0753-3322
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Qiangguyin inhibited fat accumulation in OVX mice through the p38 MAPK signaling pathway to achieve anti-osteoporosis effects

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