Neuroprotective effects of fermented tea in MPTP-induced Parkinson's disease mouse model via MAPK signaling-mediated regulation of inflammation and antioxidant activity
[Display omitted] •Semi-fermented tea exerts anti-inflammatory, anti-apoptotic, and anti-oxidant activity.•Semi-fermented tea showed the highest the level of theanine and GABA composition.•Semi-fermented tea alleviated MPTP-induced behavioral impairment and dopaminergic neuronal damage and reduced α...
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•Semi-fermented tea exerts anti-inflammatory, anti-apoptotic, and anti-oxidant activity.•Semi-fermented tea showed the highest the level of theanine and GABA composition.•Semi-fermented tea alleviated MPTP-induced behavioral impairment and dopaminergic neuronal damage and reduced α-synuclein levels.
Parkinson’s disease (PD) is a neurodegenerative disorder that is characterized by dopaminergic neuronal damage. In this study, three tea extracts from Hadong, Korea, were evaluated in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity damage model (C57BL/6 mice) for their therapeutic effects against PD: green tea (GT), semi-fermented tea (SFT), and fermented tea (FT). Theaflavin content in the teas increased but catechin content decreased with the degree of fermentation. In addition, SFT showed the highest theanine and γ-aminobutyric acid contents. SFT at a concentration of 25 μg/mL showed the highest activity in the 2,2-diphenyl-1-picrylhydrazyl radical scavenging assay among all samples. Furthermore, the 2,2′-azino-bis 3-ethylbenzothiazoline-6-sulfonic acid radical scavenging activity of 25 μg/mL SFT was higher than that of l-ascorbic acid. Fermented tea suppressed the expression of inflammatory cytokines, such as interleukin-6, tumor necrosis factor-alpha, inducible nitric oxide synthase, cyclooxygenase-2, and macrophage-1, as well as inhibited overexpression of apoptotic signals, including p-53, cleaved caspase-3, and poly (ADP-ribose) polymerase-1. Moreover, GT, SFT, and FT regulated the MPTP-induced oxidative stress-related factors, including superoxide dismutase, glutathione-S-transferase, and nicotinamide adenine dinucleotide phosphate oxidase 4. Fermented tea also alleviated MPTP-induced behavioral impairment and dopaminergic neuronal damage and reduced α-synuclein levels. These results indicate that fermented tea is effective for the treatment of neuro-inflammatory, neuro-apoptotic, and neuro-oxidative disorders. |
doi_str_mv | 10.1016/j.foodres.2022.112133 |
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•Semi-fermented tea exerts anti-inflammatory, anti-apoptotic, and anti-oxidant activity.•Semi-fermented tea showed the highest the level of theanine and GABA composition.•Semi-fermented tea alleviated MPTP-induced behavioral impairment and dopaminergic neuronal damage and reduced α-synuclein levels.
Parkinson’s disease (PD) is a neurodegenerative disorder that is characterized by dopaminergic neuronal damage. In this study, three tea extracts from Hadong, Korea, were evaluated in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity damage model (C57BL/6 mice) for their therapeutic effects against PD: green tea (GT), semi-fermented tea (SFT), and fermented tea (FT). Theaflavin content in the teas increased but catechin content decreased with the degree of fermentation. In addition, SFT showed the highest theanine and γ-aminobutyric acid contents. SFT at a concentration of 25 μg/mL showed the highest activity in the 2,2-diphenyl-1-picrylhydrazyl radical scavenging assay among all samples. Furthermore, the 2,2′-azino-bis 3-ethylbenzothiazoline-6-sulfonic acid radical scavenging activity of 25 μg/mL SFT was higher than that of l-ascorbic acid. Fermented tea suppressed the expression of inflammatory cytokines, such as interleukin-6, tumor necrosis factor-alpha, inducible nitric oxide synthase, cyclooxygenase-2, and macrophage-1, as well as inhibited overexpression of apoptotic signals, including p-53, cleaved caspase-3, and poly (ADP-ribose) polymerase-1. Moreover, GT, SFT, and FT regulated the MPTP-induced oxidative stress-related factors, including superoxide dismutase, glutathione-S-transferase, and nicotinamide adenine dinucleotide phosphate oxidase 4. Fermented tea also alleviated MPTP-induced behavioral impairment and dopaminergic neuronal damage and reduced α-synuclein levels. These results indicate that fermented tea is effective for the treatment of neuro-inflammatory, neuro-apoptotic, and neuro-oxidative disorders.</description><identifier>ISSN: 0963-9969</identifier><identifier>EISSN: 1873-7145</identifier><identifier>DOI: 10.1016/j.foodres.2022.112133</identifier><identifier>PMID: 36737888</identifier><language>eng</language><publisher>Canada: Elsevier Ltd</publisher><subject>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - therapeutic use ; Animals ; Antioxidant activity ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Inflammation - drug therapy ; Mice ; Mice, Inbred C57BL ; Neuroinflammation ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Parkinson Disease - drug therapy ; Parkinson Disease - metabolism ; Parkinson’s disease ; Semi-fermented tea ; Tea ; γ-aminobutyric acid (GABA)</subject><ispartof>Food research international, 2023-02, Vol.164, p.112133-112133, Article 112133</ispartof><rights>2022</rights><rights>Copyright © 2022. Published by Elsevier Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c280t-a04a0bc6759d3f4ff0db1bbe90487e8c998d9d07bafbaef8678499ecf049b0953</citedby><cites>FETCH-LOGICAL-c280t-a04a0bc6759d3f4ff0db1bbe90487e8c998d9d07bafbaef8678499ecf049b0953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.foodres.2022.112133$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36737888$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Yu-Rim</creatorcontrib><creatorcontrib>Moon, Gyo-Ha</creatorcontrib><creatorcontrib>Shim, Doobo</creatorcontrib><creatorcontrib>Kim, Jong Cheol</creatorcontrib><creatorcontrib>Lee, Kwon-Jai</creatorcontrib><creatorcontrib>Chung, Kang-Hyun</creatorcontrib><creatorcontrib>An, Jeung Hee</creatorcontrib><title>Neuroprotective effects of fermented tea in MPTP-induced Parkinson's disease mouse model via MAPK signaling-mediated regulation of inflammation and antioxidant activity</title><title>Food research international</title><addtitle>Food Res Int</addtitle><description>[Display omitted]
•Semi-fermented tea exerts anti-inflammatory, anti-apoptotic, and anti-oxidant activity.•Semi-fermented tea showed the highest the level of theanine and GABA composition.•Semi-fermented tea alleviated MPTP-induced behavioral impairment and dopaminergic neuronal damage and reduced α-synuclein levels.
Parkinson’s disease (PD) is a neurodegenerative disorder that is characterized by dopaminergic neuronal damage. In this study, three tea extracts from Hadong, Korea, were evaluated in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity damage model (C57BL/6 mice) for their therapeutic effects against PD: green tea (GT), semi-fermented tea (SFT), and fermented tea (FT). Theaflavin content in the teas increased but catechin content decreased with the degree of fermentation. In addition, SFT showed the highest theanine and γ-aminobutyric acid contents. SFT at a concentration of 25 μg/mL showed the highest activity in the 2,2-diphenyl-1-picrylhydrazyl radical scavenging assay among all samples. Furthermore, the 2,2′-azino-bis 3-ethylbenzothiazoline-6-sulfonic acid radical scavenging activity of 25 μg/mL SFT was higher than that of l-ascorbic acid. Fermented tea suppressed the expression of inflammatory cytokines, such as interleukin-6, tumor necrosis factor-alpha, inducible nitric oxide synthase, cyclooxygenase-2, and macrophage-1, as well as inhibited overexpression of apoptotic signals, including p-53, cleaved caspase-3, and poly (ADP-ribose) polymerase-1. Moreover, GT, SFT, and FT regulated the MPTP-induced oxidative stress-related factors, including superoxide dismutase, glutathione-S-transferase, and nicotinamide adenine dinucleotide phosphate oxidase 4. Fermented tea also alleviated MPTP-induced behavioral impairment and dopaminergic neuronal damage and reduced α-synuclein levels. These results indicate that fermented tea is effective for the treatment of neuro-inflammatory, neuro-apoptotic, and neuro-oxidative disorders.</description><subject>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - therapeutic use</subject><subject>Animals</subject><subject>Antioxidant activity</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Inflammation - drug therapy</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Neuroinflammation</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Parkinson Disease - drug therapy</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinson’s disease</subject><subject>Semi-fermented tea</subject><subject>Tea</subject><subject>γ-aminobutyric acid (GABA)</subject><issn>0963-9969</issn><issn>1873-7145</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUcFu1DAQtRCIbgufAPINLlnsOIntE6qqQhEt7KGcLccer7wkdrGTFf0jPhOHLFw52DO23sybeQ-hV5RsKaHdu8PWxWgT5G1N6npLaU0Ze4I2VHBWcdq0T9GGyI5VUnbyDJ3nfCCEdC2Xz9EZ6zjjQogN-vUF5hQfUpzATP4IGJwrWcbRYQdphDCBxRNo7AO-293vKh_sbMrfTqfvPuQY3mRsfQadAY9x_nNbGPDRa3x3ufuMs98HPfiwr0awXi_9EuznQU8-hoXHBzfocVzfOthySvrT2xKxXsby0-ML9MzpIcPLU7xA3z5c31_dVLdfP366urytTC3IVGnSaNKbjrfSMtc4R2xP-x4kaQQHYaQUVlrCe-16DU50XDRSgnGkkT2RLbtAb9e-RZMfM-RJjT4bGAYdoGynas4ZrVtG6gJtV6hJMecETj0kP-r0qChRi0nqoE4mqcUktZpU6l6fKOa-SPKv6q8rBfB-BUBZ9OghqWw8hKK6T8UcZaP_D8Vv4dKqXQ</recordid><startdate>202302</startdate><enddate>202302</enddate><creator>Lee, Yu-Rim</creator><creator>Moon, Gyo-Ha</creator><creator>Shim, Doobo</creator><creator>Kim, Jong Cheol</creator><creator>Lee, Kwon-Jai</creator><creator>Chung, Kang-Hyun</creator><creator>An, Jeung Hee</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202302</creationdate><title>Neuroprotective effects of fermented tea in MPTP-induced Parkinson's disease mouse model via MAPK signaling-mediated regulation of inflammation and antioxidant activity</title><author>Lee, Yu-Rim ; Moon, Gyo-Ha ; Shim, Doobo ; Kim, Jong Cheol ; Lee, Kwon-Jai ; Chung, Kang-Hyun ; An, Jeung Hee</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c280t-a04a0bc6759d3f4ff0db1bbe90487e8c998d9d07bafbaef8678499ecf049b0953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - therapeutic use</topic><topic>Animals</topic><topic>Antioxidant activity</topic><topic>Antioxidants - pharmacology</topic><topic>Antioxidants - therapeutic use</topic><topic>Inflammation - drug therapy</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Neuroinflammation</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Parkinson Disease - drug therapy</topic><topic>Parkinson Disease - metabolism</topic><topic>Parkinson’s disease</topic><topic>Semi-fermented tea</topic><topic>Tea</topic><topic>γ-aminobutyric acid (GABA)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Yu-Rim</creatorcontrib><creatorcontrib>Moon, Gyo-Ha</creatorcontrib><creatorcontrib>Shim, Doobo</creatorcontrib><creatorcontrib>Kim, Jong Cheol</creatorcontrib><creatorcontrib>Lee, Kwon-Jai</creatorcontrib><creatorcontrib>Chung, Kang-Hyun</creatorcontrib><creatorcontrib>An, Jeung Hee</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Food research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Yu-Rim</au><au>Moon, Gyo-Ha</au><au>Shim, Doobo</au><au>Kim, Jong Cheol</au><au>Lee, Kwon-Jai</au><au>Chung, Kang-Hyun</au><au>An, Jeung Hee</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotective effects of fermented tea in MPTP-induced Parkinson's disease mouse model via MAPK signaling-mediated regulation of inflammation and antioxidant activity</atitle><jtitle>Food research international</jtitle><addtitle>Food Res Int</addtitle><date>2023-02</date><risdate>2023</risdate><volume>164</volume><spage>112133</spage><epage>112133</epage><pages>112133-112133</pages><artnum>112133</artnum><issn>0963-9969</issn><eissn>1873-7145</eissn><abstract>[Display omitted]
•Semi-fermented tea exerts anti-inflammatory, anti-apoptotic, and anti-oxidant activity.•Semi-fermented tea showed the highest the level of theanine and GABA composition.•Semi-fermented tea alleviated MPTP-induced behavioral impairment and dopaminergic neuronal damage and reduced α-synuclein levels.
Parkinson’s disease (PD) is a neurodegenerative disorder that is characterized by dopaminergic neuronal damage. In this study, three tea extracts from Hadong, Korea, were evaluated in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity damage model (C57BL/6 mice) for their therapeutic effects against PD: green tea (GT), semi-fermented tea (SFT), and fermented tea (FT). Theaflavin content in the teas increased but catechin content decreased with the degree of fermentation. In addition, SFT showed the highest theanine and γ-aminobutyric acid contents. SFT at a concentration of 25 μg/mL showed the highest activity in the 2,2-diphenyl-1-picrylhydrazyl radical scavenging assay among all samples. Furthermore, the 2,2′-azino-bis 3-ethylbenzothiazoline-6-sulfonic acid radical scavenging activity of 25 μg/mL SFT was higher than that of l-ascorbic acid. Fermented tea suppressed the expression of inflammatory cytokines, such as interleukin-6, tumor necrosis factor-alpha, inducible nitric oxide synthase, cyclooxygenase-2, and macrophage-1, as well as inhibited overexpression of apoptotic signals, including p-53, cleaved caspase-3, and poly (ADP-ribose) polymerase-1. Moreover, GT, SFT, and FT regulated the MPTP-induced oxidative stress-related factors, including superoxide dismutase, glutathione-S-transferase, and nicotinamide adenine dinucleotide phosphate oxidase 4. Fermented tea also alleviated MPTP-induced behavioral impairment and dopaminergic neuronal damage and reduced α-synuclein levels. These results indicate that fermented tea is effective for the treatment of neuro-inflammatory, neuro-apoptotic, and neuro-oxidative disorders.</abstract><cop>Canada</cop><pub>Elsevier Ltd</pub><pmid>36737888</pmid><doi>10.1016/j.foodres.2022.112133</doi><tpages>1</tpages></addata></record> |
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subjects | 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - therapeutic use Animals Antioxidant activity Antioxidants - pharmacology Antioxidants - therapeutic use Inflammation - drug therapy Mice Mice, Inbred C57BL Neuroinflammation Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Parkinson Disease - drug therapy Parkinson Disease - metabolism Parkinson’s disease Semi-fermented tea Tea γ-aminobutyric acid (GABA) |
title | Neuroprotective effects of fermented tea in MPTP-induced Parkinson's disease mouse model via MAPK signaling-mediated regulation of inflammation and antioxidant activity |
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