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Article: Green Tea and Epigallocatechin Gallate (EGCG) for the Management of Nonalcoholic Fatty Liver Diseases (NAFLD): Insights into the Role of Oxidative Stress and Antioxidant Mechanism

TitleGreen Tea and Epigallocatechin Gallate (EGCG) for the Management of Nonalcoholic Fatty Liver Diseases (NAFLD): Insights into the Role of Oxidative Stress and Antioxidant Mechanism
Authors
Keywordsgreen tea
epigallocatechin gallate
nonalcoholic fatty liver disease
nonalcoholic steatohepatitis
multiple parallel hits
Issue Date2021
PublisherMDPI AG. The Journal's web site is located at http://www.mdpi.com/journal/antioxidants
Citation
Antioxidants, 2021, v. 10 n. 7, p. article no. 1076 How to Cite?
AbstractNonalcoholic fatty liver diseases (NAFLD) represent a set of liver disorders progressing from steatosis to steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma, which induce huge burden to human health. Many pathophysiological factors are considered to influence NAFLD in a parallel pattern, involving insulin resistance, oxidative stress, lipotoxicity, mitochondrial dysfunction, endoplasmic reticulum stress, inflammatory cascades, fibrogenic reaction, etc. However, the underlying mechanisms, including those that induce NAFLD development, have not been fully understood. Specifically, oxidative stress, mainly mediated by excessive accumulation of reactive oxygen species, has participated in the multiple NAFLD-related signaling by serving as an accelerator. Ameliorating oxidative stress and maintaining redox homeostasis may be a promising approach for the management of NAFLD. Green tea is one of the most important dietary resources of natural antioxidants, above which epigallocatechin gallate (EGCG) notably contributes to its antioxidative action. Accumulative evidence from randomized clinical trials, systematic reviews, and meta-analysis has revealed the beneficial functions of green tea and EGCG in preventing and managing NAFLD, with acceptable safety in the patients. Abundant animal and cellular studies have demonstrated that green tea and EGCG may protect against NAFLD initiation and development by alleviating oxidative stress and the related metabolism dysfunction, inflammation, fibrosis, and tumorigenesis. The targeted signaling pathways may include, but are not limited to, NRF2, AMPK, SIRT1, NF-κB, TLR4/MYD88, TGF-β/SMAD, and PI3K/Akt/FoxO1, etc. In this review, we thoroughly discuss the oxidative stress-related mechanisms involved in NAFLD development, as well as summarize the protective effects and underlying mechanisms of green tea and EGCG against NAFLD.
Persistent Identifierhttp://hdl.handle.net/10722/304842
ISSN
2023 Impact Factor: 6.0
2023 SCImago Journal Rankings: 1.222
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTANG, G-
dc.contributor.authorXu, Y-
dc.contributor.authorZHANG, C-
dc.contributor.authorWang, N-
dc.contributor.authorLi, H-
dc.contributor.authorFeng, Y-
dc.date.accessioned2021-10-05T02:35:59Z-
dc.date.available2021-10-05T02:35:59Z-
dc.date.issued2021-
dc.identifier.citationAntioxidants, 2021, v. 10 n. 7, p. article no. 1076-
dc.identifier.issn2076-3921-
dc.identifier.urihttp://hdl.handle.net/10722/304842-
dc.description.abstractNonalcoholic fatty liver diseases (NAFLD) represent a set of liver disorders progressing from steatosis to steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma, which induce huge burden to human health. Many pathophysiological factors are considered to influence NAFLD in a parallel pattern, involving insulin resistance, oxidative stress, lipotoxicity, mitochondrial dysfunction, endoplasmic reticulum stress, inflammatory cascades, fibrogenic reaction, etc. However, the underlying mechanisms, including those that induce NAFLD development, have not been fully understood. Specifically, oxidative stress, mainly mediated by excessive accumulation of reactive oxygen species, has participated in the multiple NAFLD-related signaling by serving as an accelerator. Ameliorating oxidative stress and maintaining redox homeostasis may be a promising approach for the management of NAFLD. Green tea is one of the most important dietary resources of natural antioxidants, above which epigallocatechin gallate (EGCG) notably contributes to its antioxidative action. Accumulative evidence from randomized clinical trials, systematic reviews, and meta-analysis has revealed the beneficial functions of green tea and EGCG in preventing and managing NAFLD, with acceptable safety in the patients. Abundant animal and cellular studies have demonstrated that green tea and EGCG may protect against NAFLD initiation and development by alleviating oxidative stress and the related metabolism dysfunction, inflammation, fibrosis, and tumorigenesis. The targeted signaling pathways may include, but are not limited to, NRF2, AMPK, SIRT1, NF-κB, TLR4/MYD88, TGF-β/SMAD, and PI3K/Akt/FoxO1, etc. In this review, we thoroughly discuss the oxidative stress-related mechanisms involved in NAFLD development, as well as summarize the protective effects and underlying mechanisms of green tea and EGCG against NAFLD.-
dc.languageeng-
dc.publisherMDPI AG. The Journal's web site is located at http://www.mdpi.com/journal/antioxidants-
dc.relation.ispartofAntioxidants-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectgreen tea-
dc.subjectepigallocatechin gallate-
dc.subjectnonalcoholic fatty liver disease-
dc.subjectnonalcoholic steatohepatitis-
dc.subjectmultiple parallel hits-
dc.titleGreen Tea and Epigallocatechin Gallate (EGCG) for the Management of Nonalcoholic Fatty Liver Diseases (NAFLD): Insights into the Role of Oxidative Stress and Antioxidant Mechanism-
dc.typeArticle-
dc.identifier.emailXu, Y: xyzjh@hku.hk-
dc.identifier.emailWang, N: ckwang@hku.hk-
dc.identifier.emailFeng, Y: yfeng@hku.hk-
dc.identifier.authorityWang, N=rp02075-
dc.identifier.authorityFeng, Y=rp00466-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3390/antiox10071076-
dc.identifier.pmid34356308-
dc.identifier.pmcidPMC8301033-
dc.identifier.scopuseid_2-s2.0-85116847275-
dc.identifier.hkuros326191-
dc.identifier.volume10-
dc.identifier.issue7-
dc.identifier.spagearticle no. 1076-
dc.identifier.epagearticle no. 1076-
dc.identifier.isiWOS:000675997200001-
dc.publisher.placeSwitzerland-

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