Quercetin alleviates ethanol-induced liver steatosis associated with improvement of lipophagy
Although emerging evidence demonstrated that quercetin could be explored as a potential candidate for the early intervention of alcoholic liver disease (ALD), the exact mechanisms against ethanol-induced hepatic steatosis haven't been fully elucidated. Herein, we investigated the effect of quer...
Ausführliche Beschreibung
Autor*in: |
Zeng, Hongmei [verfasserIn] Guo, Xiaoping [verfasserIn] Zhou, Feng [verfasserIn] Xiao, Lin [verfasserIn] Liu, Jingjing [verfasserIn] Jiang, Chunjie [verfasserIn] Xing, Mingyou [verfasserIn] Yao, Ping [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2018 |
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Schlagwörter: |
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Übergeordnetes Werk: |
Enthalten in: Food and chemical toxicology - New York, NY [u.a.] : Elsevier, 1982, 125, Seite 21-28 |
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Übergeordnetes Werk: |
volume:125 ; pages:21-28 |
DOI / URN: |
10.1016/j.fct.2018.12.028 |
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Katalog-ID: |
ELV001804022 |
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520 | |a Although emerging evidence demonstrated that quercetin could be explored as a potential candidate for the early intervention of alcoholic liver disease (ALD), the exact mechanisms against ethanol-induced hepatic steatosis haven't been fully elucidated. Herein, we investigated the effect of quercetin on liver steatosis caused by chronic-plus-single-binge ethanol feeding, focusing on lipophagy. Adult male mice were pair-fed with liquid diets containing ethanol (28% of total calories) and treated with quercetin for 12 weeks. Chronic-plus-binge ethanol consumption led to lipid droplets accumulation and liver damage as evidenced by histopathological changes, the increased content of triglyceride in serum and liver, and the elevated of serum ALT and AST level, which were greatly attenuated by quercetin. Moreover, quercetin blocked autophagy suppression by chronic-binge ethanol intake as manifested by the morphological improvement of mitochondrial characteristics, the increased number of autolysosome and restoration of autophagy-related protein expression. Furthermore, quercetin promoted lipophagy confirmed by the decreased perilipin 2 (PLIN2) level, activated AMPK activity and increased co-localization of liver LC3II and PLIN2 proteins. Collectively, these findings suggest that regular consumption of dietary quercetin has a role in preventing hepatic steatosis induced by chronic-plus-binge ethanol feeding, which mechanism may associate with the evident regulatory effect of quercetin on lipophagy. | ||
650 | 4 | |a Quercetin | |
650 | 4 | |a Alcoholic liver disease (ALD) | |
650 | 4 | |a Perilipin 2 (PLIN2) | |
650 | 4 | |a Lipophagy | |
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700 | 1 | |a Zhou, Feng |e verfasserin |4 aut | |
700 | 1 | |a Xiao, Lin |e verfasserin |4 aut | |
700 | 1 | |a Liu, Jingjing |e verfasserin |4 aut | |
700 | 1 | |a Jiang, Chunjie |e verfasserin |4 aut | |
700 | 1 | |a Xing, Mingyou |e verfasserin |4 aut | |
700 | 1 | |a Yao, Ping |e verfasserin |0 (orcid)0000-0002-0192-9546 |4 aut | |
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allfields |
10.1016/j.fct.2018.12.028 doi (DE-627)ELV001804022 (ELSEVIER)S0278-6915(18)30901-3 DE-627 ger DE-627 rda eng 630 640 610 DE-600 44.21 bkl Zeng, Hongmei verfasserin aut Quercetin alleviates ethanol-induced liver steatosis associated with improvement of lipophagy 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Although emerging evidence demonstrated that quercetin could be explored as a potential candidate for the early intervention of alcoholic liver disease (ALD), the exact mechanisms against ethanol-induced hepatic steatosis haven't been fully elucidated. Herein, we investigated the effect of quercetin on liver steatosis caused by chronic-plus-single-binge ethanol feeding, focusing on lipophagy. Adult male mice were pair-fed with liquid diets containing ethanol (28% of total calories) and treated with quercetin for 12 weeks. Chronic-plus-binge ethanol consumption led to lipid droplets accumulation and liver damage as evidenced by histopathological changes, the increased content of triglyceride in serum and liver, and the elevated of serum ALT and AST level, which were greatly attenuated by quercetin. Moreover, quercetin blocked autophagy suppression by chronic-binge ethanol intake as manifested by the morphological improvement of mitochondrial characteristics, the increased number of autolysosome and restoration of autophagy-related protein expression. Furthermore, quercetin promoted lipophagy confirmed by the decreased perilipin 2 (PLIN2) level, activated AMPK activity and increased co-localization of liver LC3II and PLIN2 proteins. Collectively, these findings suggest that regular consumption of dietary quercetin has a role in preventing hepatic steatosis induced by chronic-plus-binge ethanol feeding, which mechanism may associate with the evident regulatory effect of quercetin on lipophagy. Quercetin Alcoholic liver disease (ALD) Perilipin 2 (PLIN2) Lipophagy Guo, Xiaoping verfasserin aut Zhou, Feng verfasserin aut Xiao, Lin verfasserin aut Liu, Jingjing verfasserin aut Jiang, Chunjie verfasserin aut Xing, Mingyou verfasserin aut Yao, Ping verfasserin (orcid)0000-0002-0192-9546 aut Enthalten in Food and chemical toxicology New York, NY [u.a.] : Elsevier, 1982 125, Seite 21-28 Online-Ressource (DE-627)300898487 (DE-600)1483645-2 (DE-576)259270849 1873-6351 nnns volume:125 pages:21-28 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.21 Ernährung Medizin AR 125 21-28 |
spelling |
10.1016/j.fct.2018.12.028 doi (DE-627)ELV001804022 (ELSEVIER)S0278-6915(18)30901-3 DE-627 ger DE-627 rda eng 630 640 610 DE-600 44.21 bkl Zeng, Hongmei verfasserin aut Quercetin alleviates ethanol-induced liver steatosis associated with improvement of lipophagy 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Although emerging evidence demonstrated that quercetin could be explored as a potential candidate for the early intervention of alcoholic liver disease (ALD), the exact mechanisms against ethanol-induced hepatic steatosis haven't been fully elucidated. Herein, we investigated the effect of quercetin on liver steatosis caused by chronic-plus-single-binge ethanol feeding, focusing on lipophagy. Adult male mice were pair-fed with liquid diets containing ethanol (28% of total calories) and treated with quercetin for 12 weeks. Chronic-plus-binge ethanol consumption led to lipid droplets accumulation and liver damage as evidenced by histopathological changes, the increased content of triglyceride in serum and liver, and the elevated of serum ALT and AST level, which were greatly attenuated by quercetin. Moreover, quercetin blocked autophagy suppression by chronic-binge ethanol intake as manifested by the morphological improvement of mitochondrial characteristics, the increased number of autolysosome and restoration of autophagy-related protein expression. Furthermore, quercetin promoted lipophagy confirmed by the decreased perilipin 2 (PLIN2) level, activated AMPK activity and increased co-localization of liver LC3II and PLIN2 proteins. Collectively, these findings suggest that regular consumption of dietary quercetin has a role in preventing hepatic steatosis induced by chronic-plus-binge ethanol feeding, which mechanism may associate with the evident regulatory effect of quercetin on lipophagy. Quercetin Alcoholic liver disease (ALD) Perilipin 2 (PLIN2) Lipophagy Guo, Xiaoping verfasserin aut Zhou, Feng verfasserin aut Xiao, Lin verfasserin aut Liu, Jingjing verfasserin aut Jiang, Chunjie verfasserin aut Xing, Mingyou verfasserin aut Yao, Ping verfasserin (orcid)0000-0002-0192-9546 aut Enthalten in Food and chemical toxicology New York, NY [u.a.] : Elsevier, 1982 125, Seite 21-28 Online-Ressource (DE-627)300898487 (DE-600)1483645-2 (DE-576)259270849 1873-6351 nnns volume:125 pages:21-28 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.21 Ernährung Medizin AR 125 21-28 |
allfields_unstemmed |
10.1016/j.fct.2018.12.028 doi (DE-627)ELV001804022 (ELSEVIER)S0278-6915(18)30901-3 DE-627 ger DE-627 rda eng 630 640 610 DE-600 44.21 bkl Zeng, Hongmei verfasserin aut Quercetin alleviates ethanol-induced liver steatosis associated with improvement of lipophagy 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Although emerging evidence demonstrated that quercetin could be explored as a potential candidate for the early intervention of alcoholic liver disease (ALD), the exact mechanisms against ethanol-induced hepatic steatosis haven't been fully elucidated. Herein, we investigated the effect of quercetin on liver steatosis caused by chronic-plus-single-binge ethanol feeding, focusing on lipophagy. Adult male mice were pair-fed with liquid diets containing ethanol (28% of total calories) and treated with quercetin for 12 weeks. Chronic-plus-binge ethanol consumption led to lipid droplets accumulation and liver damage as evidenced by histopathological changes, the increased content of triglyceride in serum and liver, and the elevated of serum ALT and AST level, which were greatly attenuated by quercetin. Moreover, quercetin blocked autophagy suppression by chronic-binge ethanol intake as manifested by the morphological improvement of mitochondrial characteristics, the increased number of autolysosome and restoration of autophagy-related protein expression. Furthermore, quercetin promoted lipophagy confirmed by the decreased perilipin 2 (PLIN2) level, activated AMPK activity and increased co-localization of liver LC3II and PLIN2 proteins. Collectively, these findings suggest that regular consumption of dietary quercetin has a role in preventing hepatic steatosis induced by chronic-plus-binge ethanol feeding, which mechanism may associate with the evident regulatory effect of quercetin on lipophagy. Quercetin Alcoholic liver disease (ALD) Perilipin 2 (PLIN2) Lipophagy Guo, Xiaoping verfasserin aut Zhou, Feng verfasserin aut Xiao, Lin verfasserin aut Liu, Jingjing verfasserin aut Jiang, Chunjie verfasserin aut Xing, Mingyou verfasserin aut Yao, Ping verfasserin (orcid)0000-0002-0192-9546 aut Enthalten in Food and chemical toxicology New York, NY [u.a.] : Elsevier, 1982 125, Seite 21-28 Online-Ressource (DE-627)300898487 (DE-600)1483645-2 (DE-576)259270849 1873-6351 nnns volume:125 pages:21-28 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.21 Ernährung Medizin AR 125 21-28 |
allfieldsGer |
10.1016/j.fct.2018.12.028 doi (DE-627)ELV001804022 (ELSEVIER)S0278-6915(18)30901-3 DE-627 ger DE-627 rda eng 630 640 610 DE-600 44.21 bkl Zeng, Hongmei verfasserin aut Quercetin alleviates ethanol-induced liver steatosis associated with improvement of lipophagy 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Although emerging evidence demonstrated that quercetin could be explored as a potential candidate for the early intervention of alcoholic liver disease (ALD), the exact mechanisms against ethanol-induced hepatic steatosis haven't been fully elucidated. Herein, we investigated the effect of quercetin on liver steatosis caused by chronic-plus-single-binge ethanol feeding, focusing on lipophagy. Adult male mice were pair-fed with liquid diets containing ethanol (28% of total calories) and treated with quercetin for 12 weeks. Chronic-plus-binge ethanol consumption led to lipid droplets accumulation and liver damage as evidenced by histopathological changes, the increased content of triglyceride in serum and liver, and the elevated of serum ALT and AST level, which were greatly attenuated by quercetin. Moreover, quercetin blocked autophagy suppression by chronic-binge ethanol intake as manifested by the morphological improvement of mitochondrial characteristics, the increased number of autolysosome and restoration of autophagy-related protein expression. Furthermore, quercetin promoted lipophagy confirmed by the decreased perilipin 2 (PLIN2) level, activated AMPK activity and increased co-localization of liver LC3II and PLIN2 proteins. Collectively, these findings suggest that regular consumption of dietary quercetin has a role in preventing hepatic steatosis induced by chronic-plus-binge ethanol feeding, which mechanism may associate with the evident regulatory effect of quercetin on lipophagy. Quercetin Alcoholic liver disease (ALD) Perilipin 2 (PLIN2) Lipophagy Guo, Xiaoping verfasserin aut Zhou, Feng verfasserin aut Xiao, Lin verfasserin aut Liu, Jingjing verfasserin aut Jiang, Chunjie verfasserin aut Xing, Mingyou verfasserin aut Yao, Ping verfasserin (orcid)0000-0002-0192-9546 aut Enthalten in Food and chemical toxicology New York, NY [u.a.] : Elsevier, 1982 125, Seite 21-28 Online-Ressource (DE-627)300898487 (DE-600)1483645-2 (DE-576)259270849 1873-6351 nnns volume:125 pages:21-28 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.21 Ernährung Medizin AR 125 21-28 |
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10.1016/j.fct.2018.12.028 doi (DE-627)ELV001804022 (ELSEVIER)S0278-6915(18)30901-3 DE-627 ger DE-627 rda eng 630 640 610 DE-600 44.21 bkl Zeng, Hongmei verfasserin aut Quercetin alleviates ethanol-induced liver steatosis associated with improvement of lipophagy 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Although emerging evidence demonstrated that quercetin could be explored as a potential candidate for the early intervention of alcoholic liver disease (ALD), the exact mechanisms against ethanol-induced hepatic steatosis haven't been fully elucidated. Herein, we investigated the effect of quercetin on liver steatosis caused by chronic-plus-single-binge ethanol feeding, focusing on lipophagy. Adult male mice were pair-fed with liquid diets containing ethanol (28% of total calories) and treated with quercetin for 12 weeks. Chronic-plus-binge ethanol consumption led to lipid droplets accumulation and liver damage as evidenced by histopathological changes, the increased content of triglyceride in serum and liver, and the elevated of serum ALT and AST level, which were greatly attenuated by quercetin. Moreover, quercetin blocked autophagy suppression by chronic-binge ethanol intake as manifested by the morphological improvement of mitochondrial characteristics, the increased number of autolysosome and restoration of autophagy-related protein expression. Furthermore, quercetin promoted lipophagy confirmed by the decreased perilipin 2 (PLIN2) level, activated AMPK activity and increased co-localization of liver LC3II and PLIN2 proteins. Collectively, these findings suggest that regular consumption of dietary quercetin has a role in preventing hepatic steatosis induced by chronic-plus-binge ethanol feeding, which mechanism may associate with the evident regulatory effect of quercetin on lipophagy. Quercetin Alcoholic liver disease (ALD) Perilipin 2 (PLIN2) Lipophagy Guo, Xiaoping verfasserin aut Zhou, Feng verfasserin aut Xiao, Lin verfasserin aut Liu, Jingjing verfasserin aut Jiang, Chunjie verfasserin aut Xing, Mingyou verfasserin aut Yao, Ping verfasserin (orcid)0000-0002-0192-9546 aut Enthalten in Food and chemical toxicology New York, NY [u.a.] : Elsevier, 1982 125, Seite 21-28 Online-Ressource (DE-627)300898487 (DE-600)1483645-2 (DE-576)259270849 1873-6351 nnns volume:125 pages:21-28 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.21 Ernährung Medizin AR 125 21-28 |
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630 640 610 DE-600 44.21 bkl Quercetin alleviates ethanol-induced liver steatosis associated with improvement of lipophagy Quercetin Alcoholic liver disease (ALD) Perilipin 2 (PLIN2) Lipophagy |
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Zeng, Hongmei Guo, Xiaoping Zhou, Feng Xiao, Lin Liu, Jingjing Jiang, Chunjie Xing, Mingyou Yao, Ping |
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quercetin alleviates ethanol-induced liver steatosis associated with improvement of lipophagy |
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Quercetin alleviates ethanol-induced liver steatosis associated with improvement of lipophagy |
abstract |
Although emerging evidence demonstrated that quercetin could be explored as a potential candidate for the early intervention of alcoholic liver disease (ALD), the exact mechanisms against ethanol-induced hepatic steatosis haven't been fully elucidated. Herein, we investigated the effect of quercetin on liver steatosis caused by chronic-plus-single-binge ethanol feeding, focusing on lipophagy. Adult male mice were pair-fed with liquid diets containing ethanol (28% of total calories) and treated with quercetin for 12 weeks. Chronic-plus-binge ethanol consumption led to lipid droplets accumulation and liver damage as evidenced by histopathological changes, the increased content of triglyceride in serum and liver, and the elevated of serum ALT and AST level, which were greatly attenuated by quercetin. Moreover, quercetin blocked autophagy suppression by chronic-binge ethanol intake as manifested by the morphological improvement of mitochondrial characteristics, the increased number of autolysosome and restoration of autophagy-related protein expression. Furthermore, quercetin promoted lipophagy confirmed by the decreased perilipin 2 (PLIN2) level, activated AMPK activity and increased co-localization of liver LC3II and PLIN2 proteins. Collectively, these findings suggest that regular consumption of dietary quercetin has a role in preventing hepatic steatosis induced by chronic-plus-binge ethanol feeding, which mechanism may associate with the evident regulatory effect of quercetin on lipophagy. |
abstractGer |
Although emerging evidence demonstrated that quercetin could be explored as a potential candidate for the early intervention of alcoholic liver disease (ALD), the exact mechanisms against ethanol-induced hepatic steatosis haven't been fully elucidated. Herein, we investigated the effect of quercetin on liver steatosis caused by chronic-plus-single-binge ethanol feeding, focusing on lipophagy. Adult male mice were pair-fed with liquid diets containing ethanol (28% of total calories) and treated with quercetin for 12 weeks. Chronic-plus-binge ethanol consumption led to lipid droplets accumulation and liver damage as evidenced by histopathological changes, the increased content of triglyceride in serum and liver, and the elevated of serum ALT and AST level, which were greatly attenuated by quercetin. Moreover, quercetin blocked autophagy suppression by chronic-binge ethanol intake as manifested by the morphological improvement of mitochondrial characteristics, the increased number of autolysosome and restoration of autophagy-related protein expression. Furthermore, quercetin promoted lipophagy confirmed by the decreased perilipin 2 (PLIN2) level, activated AMPK activity and increased co-localization of liver LC3II and PLIN2 proteins. Collectively, these findings suggest that regular consumption of dietary quercetin has a role in preventing hepatic steatosis induced by chronic-plus-binge ethanol feeding, which mechanism may associate with the evident regulatory effect of quercetin on lipophagy. |
abstract_unstemmed |
Although emerging evidence demonstrated that quercetin could be explored as a potential candidate for the early intervention of alcoholic liver disease (ALD), the exact mechanisms against ethanol-induced hepatic steatosis haven't been fully elucidated. Herein, we investigated the effect of quercetin on liver steatosis caused by chronic-plus-single-binge ethanol feeding, focusing on lipophagy. Adult male mice were pair-fed with liquid diets containing ethanol (28% of total calories) and treated with quercetin for 12 weeks. Chronic-plus-binge ethanol consumption led to lipid droplets accumulation and liver damage as evidenced by histopathological changes, the increased content of triglyceride in serum and liver, and the elevated of serum ALT and AST level, which were greatly attenuated by quercetin. Moreover, quercetin blocked autophagy suppression by chronic-binge ethanol intake as manifested by the morphological improvement of mitochondrial characteristics, the increased number of autolysosome and restoration of autophagy-related protein expression. Furthermore, quercetin promoted lipophagy confirmed by the decreased perilipin 2 (PLIN2) level, activated AMPK activity and increased co-localization of liver LC3II and PLIN2 proteins. Collectively, these findings suggest that regular consumption of dietary quercetin has a role in preventing hepatic steatosis induced by chronic-plus-binge ethanol feeding, which mechanism may associate with the evident regulatory effect of quercetin on lipophagy. |
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