Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway

Que Zui tea (QT) is an important herbal tea in the diet of the ‘Yi’ people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from Q...
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Autor*in:	Yongchao Wang [verfasserIn] Yongpeng Wang [verfasserIn] Tianrui Zhao [verfasserIn] Mengcheng Li [verfasserIn] Yudan Wang [verfasserIn] Jianxin Cao [verfasserIn] Yaping Liu [verfasserIn] Zhengxuan Wang [verfasserIn] Guiguang Cheng [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2024

Schlagwörter:	Que Zui tea oxidative stress apoptosis SIRT1/Nrf2 signaling pathway

Übergeordnetes Werk:	In: Molecules - MDPI AG, 2003, 29(2024), 6, p 1384
Übergeordnetes Werk:	volume:29 ; year:2024 ; number:6, p 1384

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/molecules29061384

Katalog-ID:	DOAJ100456294

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allfields	10.3390/molecules29061384 doi (DE-627)DOAJ100456294 (DE-599)DOAJad0f6b0bdc424df7b7b5131978fe4dfc DE-627 ger DE-627 rakwb eng QD241-441 Yongchao Wang verfasserin aut Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Que Zui tea (QT) is an important herbal tea in the diet of the ‘Yi’ people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from QT against ᴅ-galactose (ᴅ-gal)-induced oxidative stress damage in mice and its potential mechanisms. QE was identified as UHPLC-HRMS/MS for its chemical composition and possible bioactive substances. Thus, QE is rich in phenolic and flavonoid compounds. Twelve compounds were identified, the main components of which were chlorogenic acid, quinic acid, and 6′-<i<O</i<-caffeoylarbutin. Histopathological and biochemical analysis revealed that QE significantly alleviated brain, liver, and kidney damage in ᴅ-gal-treated mice. Moreover, QE remarkably attenuated oxidative stress by activating the Nrf2/HO-1 pathway to increase the expression of antioxidant indexes, including GSH, GSH-Px, CAT, SOD, and T-AOC. In addition, QE administration could inhibit the IL-1β and IL-6 levels, which suppress the inflammatory response. QE could noticeably alleviate apoptosis by inhibiting the expressions of Caspase-3 and Bax proteins in the brains, livers, and kidneys of mice. The anti-apoptosis mechanism may be related to the upregulation of the SIRT1 protein and the downregulation of the p53 protein induced by QE in the brain, liver, and kidney tissues of mice. Molecular docking analysis demonstrated that the main components of QE, 6′-<i<O</i<-caffeoylarbutin, chlorogenic acid, quinic acid, and robustaside A, had good binding ability with Nrf2 and SIRT1 proteins. The present study indicated that QE could alleviate ᴅ-gal-induced brain, liver and kidney damage in mice by inhibiting the oxidative stress and cell apoptosis; additionally, the potential mechanism may be associated with the SIRT1/Nrf2 signaling pathway. Que Zui tea oxidative stress apoptosis SIRT1/Nrf2 signaling pathway Organic chemistry Yongpeng Wang verfasserin aut Tianrui Zhao verfasserin aut Mengcheng Li verfasserin aut Yudan Wang verfasserin aut Jianxin Cao verfasserin aut Yaping Liu verfasserin aut Zhengxuan Wang verfasserin aut Guiguang Cheng verfasserin aut In Molecules MDPI AG, 2003 29(2024), 6, p 1384 (DE-627)311313132 (DE-600)2008644-1 14203049 nnns volume:29 year:2024 number:6, p 1384 https://doi.org/10.3390/molecules29061384 kostenfrei https://doaj.org/article/ad0f6b0bdc424df7b7b5131978fe4dfc kostenfrei https://www.mdpi.com/1420-3049/29/6/1384 kostenfrei https://doaj.org/toc/1420-3049 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 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_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 29 2024 6, p 1384
spelling	10.3390/molecules29061384 doi (DE-627)DOAJ100456294 (DE-599)DOAJad0f6b0bdc424df7b7b5131978fe4dfc DE-627 ger DE-627 rakwb eng QD241-441 Yongchao Wang verfasserin aut Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Que Zui tea (QT) is an important herbal tea in the diet of the ‘Yi’ people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from QT against ᴅ-galactose (ᴅ-gal)-induced oxidative stress damage in mice and its potential mechanisms. QE was identified as UHPLC-HRMS/MS for its chemical composition and possible bioactive substances. Thus, QE is rich in phenolic and flavonoid compounds. Twelve compounds were identified, the main components of which were chlorogenic acid, quinic acid, and 6′-<i<O</i<-caffeoylarbutin. Histopathological and biochemical analysis revealed that QE significantly alleviated brain, liver, and kidney damage in ᴅ-gal-treated mice. Moreover, QE remarkably attenuated oxidative stress by activating the Nrf2/HO-1 pathway to increase the expression of antioxidant indexes, including GSH, GSH-Px, CAT, SOD, and T-AOC. In addition, QE administration could inhibit the IL-1β and IL-6 levels, which suppress the inflammatory response. QE could noticeably alleviate apoptosis by inhibiting the expressions of Caspase-3 and Bax proteins in the brains, livers, and kidneys of mice. The anti-apoptosis mechanism may be related to the upregulation of the SIRT1 protein and the downregulation of the p53 protein induced by QE in the brain, liver, and kidney tissues of mice. Molecular docking analysis demonstrated that the main components of QE, 6′-<i<O</i<-caffeoylarbutin, chlorogenic acid, quinic acid, and robustaside A, had good binding ability with Nrf2 and SIRT1 proteins. The present study indicated that QE could alleviate ᴅ-gal-induced brain, liver and kidney damage in mice by inhibiting the oxidative stress and cell apoptosis; additionally, the potential mechanism may be associated with the SIRT1/Nrf2 signaling pathway. Que Zui tea oxidative stress apoptosis SIRT1/Nrf2 signaling pathway Organic chemistry Yongpeng Wang verfasserin aut Tianrui Zhao verfasserin aut Mengcheng Li verfasserin aut Yudan Wang verfasserin aut Jianxin Cao verfasserin aut Yaping Liu verfasserin aut Zhengxuan Wang verfasserin aut Guiguang Cheng verfasserin aut In Molecules MDPI AG, 2003 29(2024), 6, p 1384 (DE-627)311313132 (DE-600)2008644-1 14203049 nnns volume:29 year:2024 number:6, p 1384 https://doi.org/10.3390/molecules29061384 kostenfrei https://doaj.org/article/ad0f6b0bdc424df7b7b5131978fe4dfc kostenfrei https://www.mdpi.com/1420-3049/29/6/1384 kostenfrei https://doaj.org/toc/1420-3049 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 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_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 29 2024 6, p 1384
allfields_unstemmed	10.3390/molecules29061384 doi (DE-627)DOAJ100456294 (DE-599)DOAJad0f6b0bdc424df7b7b5131978fe4dfc DE-627 ger DE-627 rakwb eng QD241-441 Yongchao Wang verfasserin aut Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Que Zui tea (QT) is an important herbal tea in the diet of the ‘Yi’ people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from QT against ᴅ-galactose (ᴅ-gal)-induced oxidative stress damage in mice and its potential mechanisms. QE was identified as UHPLC-HRMS/MS for its chemical composition and possible bioactive substances. Thus, QE is rich in phenolic and flavonoid compounds. Twelve compounds were identified, the main components of which were chlorogenic acid, quinic acid, and 6′-<i<O</i<-caffeoylarbutin. Histopathological and biochemical analysis revealed that QE significantly alleviated brain, liver, and kidney damage in ᴅ-gal-treated mice. Moreover, QE remarkably attenuated oxidative stress by activating the Nrf2/HO-1 pathway to increase the expression of antioxidant indexes, including GSH, GSH-Px, CAT, SOD, and T-AOC. In addition, QE administration could inhibit the IL-1β and IL-6 levels, which suppress the inflammatory response. QE could noticeably alleviate apoptosis by inhibiting the expressions of Caspase-3 and Bax proteins in the brains, livers, and kidneys of mice. The anti-apoptosis mechanism may be related to the upregulation of the SIRT1 protein and the downregulation of the p53 protein induced by QE in the brain, liver, and kidney tissues of mice. Molecular docking analysis demonstrated that the main components of QE, 6′-<i<O</i<-caffeoylarbutin, chlorogenic acid, quinic acid, and robustaside A, had good binding ability with Nrf2 and SIRT1 proteins. The present study indicated that QE could alleviate ᴅ-gal-induced brain, liver and kidney damage in mice by inhibiting the oxidative stress and cell apoptosis; additionally, the potential mechanism may be associated with the SIRT1/Nrf2 signaling pathway. Que Zui tea oxidative stress apoptosis SIRT1/Nrf2 signaling pathway Organic chemistry Yongpeng Wang verfasserin aut Tianrui Zhao verfasserin aut Mengcheng Li verfasserin aut Yudan Wang verfasserin aut Jianxin Cao verfasserin aut Yaping Liu verfasserin aut Zhengxuan Wang verfasserin aut Guiguang Cheng verfasserin aut In Molecules MDPI AG, 2003 29(2024), 6, p 1384 (DE-627)311313132 (DE-600)2008644-1 14203049 nnns volume:29 year:2024 number:6, p 1384 https://doi.org/10.3390/molecules29061384 kostenfrei https://doaj.org/article/ad0f6b0bdc424df7b7b5131978fe4dfc kostenfrei https://www.mdpi.com/1420-3049/29/6/1384 kostenfrei https://doaj.org/toc/1420-3049 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 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_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 29 2024 6, p 1384
allfieldsGer	10.3390/molecules29061384 doi (DE-627)DOAJ100456294 (DE-599)DOAJad0f6b0bdc424df7b7b5131978fe4dfc DE-627 ger DE-627 rakwb eng QD241-441 Yongchao Wang verfasserin aut Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Que Zui tea (QT) is an important herbal tea in the diet of the ‘Yi’ people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from QT against ᴅ-galactose (ᴅ-gal)-induced oxidative stress damage in mice and its potential mechanisms. QE was identified as UHPLC-HRMS/MS for its chemical composition and possible bioactive substances. Thus, QE is rich in phenolic and flavonoid compounds. Twelve compounds were identified, the main components of which were chlorogenic acid, quinic acid, and 6′-<i<O</i<-caffeoylarbutin. Histopathological and biochemical analysis revealed that QE significantly alleviated brain, liver, and kidney damage in ᴅ-gal-treated mice. Moreover, QE remarkably attenuated oxidative stress by activating the Nrf2/HO-1 pathway to increase the expression of antioxidant indexes, including GSH, GSH-Px, CAT, SOD, and T-AOC. In addition, QE administration could inhibit the IL-1β and IL-6 levels, which suppress the inflammatory response. QE could noticeably alleviate apoptosis by inhibiting the expressions of Caspase-3 and Bax proteins in the brains, livers, and kidneys of mice. The anti-apoptosis mechanism may be related to the upregulation of the SIRT1 protein and the downregulation of the p53 protein induced by QE in the brain, liver, and kidney tissues of mice. Molecular docking analysis demonstrated that the main components of QE, 6′-<i<O</i<-caffeoylarbutin, chlorogenic acid, quinic acid, and robustaside A, had good binding ability with Nrf2 and SIRT1 proteins. The present study indicated that QE could alleviate ᴅ-gal-induced brain, liver and kidney damage in mice by inhibiting the oxidative stress and cell apoptosis; additionally, the potential mechanism may be associated with the SIRT1/Nrf2 signaling pathway. Que Zui tea oxidative stress apoptosis SIRT1/Nrf2 signaling pathway Organic chemistry Yongpeng Wang verfasserin aut Tianrui Zhao verfasserin aut Mengcheng Li verfasserin aut Yudan Wang verfasserin aut Jianxin Cao verfasserin aut Yaping Liu verfasserin aut Zhengxuan Wang verfasserin aut Guiguang Cheng verfasserin aut In Molecules MDPI AG, 2003 29(2024), 6, p 1384 (DE-627)311313132 (DE-600)2008644-1 14203049 nnns volume:29 year:2024 number:6, p 1384 https://doi.org/10.3390/molecules29061384 kostenfrei https://doaj.org/article/ad0f6b0bdc424df7b7b5131978fe4dfc kostenfrei https://www.mdpi.com/1420-3049/29/6/1384 kostenfrei https://doaj.org/toc/1420-3049 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 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_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 29 2024 6, p 1384
allfieldsSound	10.3390/molecules29061384 doi (DE-627)DOAJ100456294 (DE-599)DOAJad0f6b0bdc424df7b7b5131978fe4dfc DE-627 ger DE-627 rakwb eng QD241-441 Yongchao Wang verfasserin aut Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Que Zui tea (QT) is an important herbal tea in the diet of the ‘Yi’ people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from QT against ᴅ-galactose (ᴅ-gal)-induced oxidative stress damage in mice and its potential mechanisms. QE was identified as UHPLC-HRMS/MS for its chemical composition and possible bioactive substances. Thus, QE is rich in phenolic and flavonoid compounds. Twelve compounds were identified, the main components of which were chlorogenic acid, quinic acid, and 6′-<i<O</i<-caffeoylarbutin. Histopathological and biochemical analysis revealed that QE significantly alleviated brain, liver, and kidney damage in ᴅ-gal-treated mice. Moreover, QE remarkably attenuated oxidative stress by activating the Nrf2/HO-1 pathway to increase the expression of antioxidant indexes, including GSH, GSH-Px, CAT, SOD, and T-AOC. In addition, QE administration could inhibit the IL-1β and IL-6 levels, which suppress the inflammatory response. QE could noticeably alleviate apoptosis by inhibiting the expressions of Caspase-3 and Bax proteins in the brains, livers, and kidneys of mice. The anti-apoptosis mechanism may be related to the upregulation of the SIRT1 protein and the downregulation of the p53 protein induced by QE in the brain, liver, and kidney tissues of mice. Molecular docking analysis demonstrated that the main components of QE, 6′-<i<O</i<-caffeoylarbutin, chlorogenic acid, quinic acid, and robustaside A, had good binding ability with Nrf2 and SIRT1 proteins. The present study indicated that QE could alleviate ᴅ-gal-induced brain, liver and kidney damage in mice by inhibiting the oxidative stress and cell apoptosis; additionally, the potential mechanism may be associated with the SIRT1/Nrf2 signaling pathway. Que Zui tea oxidative stress apoptosis SIRT1/Nrf2 signaling pathway Organic chemistry Yongpeng Wang verfasserin aut Tianrui Zhao verfasserin aut Mengcheng Li verfasserin aut Yudan Wang verfasserin aut Jianxin Cao verfasserin aut Yaping Liu verfasserin aut Zhengxuan Wang verfasserin aut Guiguang Cheng verfasserin aut In Molecules MDPI AG, 2003 29(2024), 6, p 1384 (DE-627)311313132 (DE-600)2008644-1 14203049 nnns volume:29 year:2024 number:6, p 1384 https://doi.org/10.3390/molecules29061384 kostenfrei https://doaj.org/article/ad0f6b0bdc424df7b7b5131978fe4dfc kostenfrei https://www.mdpi.com/1420-3049/29/6/1384 kostenfrei https://doaj.org/toc/1420-3049 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 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_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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 29 2024 6, p 1384
language	English
source	In Molecules 29(2024), 6, p 1384 volume:29 year:2024 number:6, p 1384
sourceStr	In Molecules 29(2024), 6, p 1384 volume:29 year:2024 number:6, p 1384
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Que Zui tea oxidative stress apoptosis SIRT1/Nrf2 signaling pathway Organic chemistry
isfreeaccess_bool	true
container_title	Molecules
authorswithroles_txt_mv	Yongchao Wang @@aut@@ Yongpeng Wang @@aut@@ Tianrui Zhao @@aut@@ Mengcheng Li @@aut@@ Yudan Wang @@aut@@ Jianxin Cao @@aut@@ Yaping Liu @@aut@@ Zhengxuan Wang @@aut@@ Guiguang Cheng @@aut@@
publishDateDaySort_date	2024-01-01T00:00:00Z
hierarchy_top_id	311313132
id	DOAJ100456294
language_de	englisch
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callnumber-first	Q - Science
author	Yongchao Wang
spellingShingle	Yongchao Wang misc QD241-441 misc Que Zui tea misc oxidative stress misc apoptosis misc SIRT1/Nrf2 signaling pathway misc Organic chemistry Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway
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topic_title	QD241-441 Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway Que Zui tea oxidative stress apoptosis SIRT1/Nrf2 signaling pathway
topic	misc QD241-441 misc Que Zui tea misc oxidative stress misc apoptosis misc SIRT1/Nrf2 signaling pathway misc Organic chemistry
topic_unstemmed	misc QD241-441 misc Que Zui tea misc oxidative stress misc apoptosis misc SIRT1/Nrf2 signaling pathway misc Organic chemistry
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title	Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway
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title_full	Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway
author_sort	Yongchao Wang
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author_browse	Yongchao Wang Yongpeng Wang Tianrui Zhao Mengcheng Li Yudan Wang Jianxin Cao Yaping Liu Zhengxuan Wang Guiguang Cheng
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title_sort	protective effect of que zui tea on <span style="font-variant: small-caps"<d</span<-galactose-induced oxidative stress damage in mice via regulating sirt1/nrf2 signaling pathway
callnumber	QD241-441
title_auth	Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway
abstract	Que Zui tea (QT) is an important herbal tea in the diet of the ‘Yi’ people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from QT against ᴅ-galactose (ᴅ-gal)-induced oxidative stress damage in mice and its potential mechanisms. QE was identified as UHPLC-HRMS/MS for its chemical composition and possible bioactive substances. Thus, QE is rich in phenolic and flavonoid compounds. Twelve compounds were identified, the main components of which were chlorogenic acid, quinic acid, and 6′-<i<O</i<-caffeoylarbutin. Histopathological and biochemical analysis revealed that QE significantly alleviated brain, liver, and kidney damage in ᴅ-gal-treated mice. Moreover, QE remarkably attenuated oxidative stress by activating the Nrf2/HO-1 pathway to increase the expression of antioxidant indexes, including GSH, GSH-Px, CAT, SOD, and T-AOC. In addition, QE administration could inhibit the IL-1β and IL-6 levels, which suppress the inflammatory response. QE could noticeably alleviate apoptosis by inhibiting the expressions of Caspase-3 and Bax proteins in the brains, livers, and kidneys of mice. The anti-apoptosis mechanism may be related to the upregulation of the SIRT1 protein and the downregulation of the p53 protein induced by QE in the brain, liver, and kidney tissues of mice. Molecular docking analysis demonstrated that the main components of QE, 6′-<i<O</i<-caffeoylarbutin, chlorogenic acid, quinic acid, and robustaside A, had good binding ability with Nrf2 and SIRT1 proteins. The present study indicated that QE could alleviate ᴅ-gal-induced brain, liver and kidney damage in mice by inhibiting the oxidative stress and cell apoptosis; additionally, the potential mechanism may be associated with the SIRT1/Nrf2 signaling pathway.
abstractGer	Que Zui tea (QT) is an important herbal tea in the diet of the ‘Yi’ people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from QT against ᴅ-galactose (ᴅ-gal)-induced oxidative stress damage in mice and its potential mechanisms. QE was identified as UHPLC-HRMS/MS for its chemical composition and possible bioactive substances. Thus, QE is rich in phenolic and flavonoid compounds. Twelve compounds were identified, the main components of which were chlorogenic acid, quinic acid, and 6′-<i<O</i<-caffeoylarbutin. Histopathological and biochemical analysis revealed that QE significantly alleviated brain, liver, and kidney damage in ᴅ-gal-treated mice. Moreover, QE remarkably attenuated oxidative stress by activating the Nrf2/HO-1 pathway to increase the expression of antioxidant indexes, including GSH, GSH-Px, CAT, SOD, and T-AOC. In addition, QE administration could inhibit the IL-1β and IL-6 levels, which suppress the inflammatory response. QE could noticeably alleviate apoptosis by inhibiting the expressions of Caspase-3 and Bax proteins in the brains, livers, and kidneys of mice. The anti-apoptosis mechanism may be related to the upregulation of the SIRT1 protein and the downregulation of the p53 protein induced by QE in the brain, liver, and kidney tissues of mice. Molecular docking analysis demonstrated that the main components of QE, 6′-<i<O</i<-caffeoylarbutin, chlorogenic acid, quinic acid, and robustaside A, had good binding ability with Nrf2 and SIRT1 proteins. The present study indicated that QE could alleviate ᴅ-gal-induced brain, liver and kidney damage in mice by inhibiting the oxidative stress and cell apoptosis; additionally, the potential mechanism may be associated with the SIRT1/Nrf2 signaling pathway.
abstract_unstemmed	Que Zui tea (QT) is an important herbal tea in the diet of the ‘Yi’ people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from QT against ᴅ-galactose (ᴅ-gal)-induced oxidative stress damage in mice and its potential mechanisms. QE was identified as UHPLC-HRMS/MS for its chemical composition and possible bioactive substances. Thus, QE is rich in phenolic and flavonoid compounds. Twelve compounds were identified, the main components of which were chlorogenic acid, quinic acid, and 6′-<i<O</i<-caffeoylarbutin. Histopathological and biochemical analysis revealed that QE significantly alleviated brain, liver, and kidney damage in ᴅ-gal-treated mice. Moreover, QE remarkably attenuated oxidative stress by activating the Nrf2/HO-1 pathway to increase the expression of antioxidant indexes, including GSH, GSH-Px, CAT, SOD, and T-AOC. In addition, QE administration could inhibit the IL-1β and IL-6 levels, which suppress the inflammatory response. QE could noticeably alleviate apoptosis by inhibiting the expressions of Caspase-3 and Bax proteins in the brains, livers, and kidneys of mice. The anti-apoptosis mechanism may be related to the upregulation of the SIRT1 protein and the downregulation of the p53 protein induced by QE in the brain, liver, and kidney tissues of mice. Molecular docking analysis demonstrated that the main components of QE, 6′-<i<O</i<-caffeoylarbutin, chlorogenic acid, quinic acid, and robustaside A, had good binding ability with Nrf2 and SIRT1 proteins. The present study indicated that QE could alleviate ᴅ-gal-induced brain, liver and kidney damage in mice by inhibiting the oxidative stress and cell apoptosis; additionally, the potential mechanism may be associated with the SIRT1/Nrf2 signaling pathway.
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title_short	Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway
url	https://doi.org/10.3390/molecules29061384 https://doaj.org/article/ad0f6b0bdc424df7b7b5131978fe4dfc https://www.mdpi.com/1420-3049/29/6/1384 https://doaj.org/toc/1420-3049
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Protective Effect of Que Zui Tea on <span style="font-variant: small-caps"<d</span<-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway

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