Effects of (−)-epicatechin on neuroinflammation and hyperphosphorylation of tau in the hippocampus of aged mice
Evidence has implicated oxidative stress (OS) and inflammation as drivers of neurodegenerative pathologies. We previously reported on the beneficial effects of (−)-epicatechin (Epi) treatment on aging-induced OS and its capacity to restore modulators of mitochondrial biogenesis in the prefrontal cor...
Saved in:
Published in | Food & function Vol. 11; no. 12; pp. 1351 - 1361 |
---|---|
Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Royal Society of Chemistry
01.12.2020
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | Evidence has implicated oxidative stress (OS) and inflammation as drivers of neurodegenerative pathologies. We previously reported on the beneficial effects of (−)-epicatechin (Epi) treatment on aging-induced OS and its capacity to restore modulators of mitochondrial biogenesis in the prefrontal cortex of 26-month-old male mice. In the present study using the same mouse model of aging, we examined the capacity of Epi to mitigate hippocampus OS, inflammation, hyperphosphorylation of tau protein, soluble β-amyloid protein levels, cell survival, memory, anxiety-like behavior levels and systemic inflammation. Mice were subjected to 4 weeks of Epi treatment (1 mg kg
−1
day
−1
) and samples of the hippocampus were obtained. Assessments of the OS markers, protein carbonyls, and malondialdehyde levels demonstrated their significant increase (∼3 fold) with aging that were partially suppressed by Epi. The protein levels of the glial fibrillary acidic protein, inflammatory factor 1 (Iba1), pro-inflammatory cytokines, interleukins (IL-1β, IL-3, 5, 6 and 15), cyclooxygenase 2, tumor necrosis factor α, nuclear factor-activated B cells and interferon γ increase with aging and were also significantly decreased with Epi treatment. However, anti-inflammatory cytokines, IL-1ra, IL-10 and 11 decrease with aging and were restored with Epi. Epi also reversed the aging effects on the hyperphosphorylation of tau, increased soluble β-amyloid levels (∼2 fold), cellular death (as per caspase 3 and 9 activity), and reduced nerve growth factor and triggering receptor expressed on myeloid cells 2 levels. Measures of anxiety like-behavior and memory demonstrated improvements with Epi treatment. Indicators of systemic inflammation increase with aging and Epi was capable of decreasing blood inflammatory markers. Altogether, the results show a significant capacity of Epi to mitigate hippocampus OS and inflammation leading to improved brain function.
(−)-Epicatechin reduces neuroinflammation and Tau-hp, improving memory and learning. |
---|---|
AbstractList | Evidence has implicated oxidative stress (OS) and inflammation as drivers of neurodegenerative pathologies. We previously reported on the beneficial effects of (−)-epicatechin (Epi) treatment on aging-induced OS and its capacity to restore modulators of mitochondrial biogenesis in the prefrontal cortex of 26-month-old male mice. In the present study using the same mouse model of aging, we examined the capacity of Epi to mitigate hippocampus OS, inflammation, hyperphosphorylation of tau protein, soluble β-amyloid protein levels, cell survival, memory, anxiety-like behavior levels and systemic inflammation. Mice were subjected to 4 weeks of Epi treatment (1 mg kg
−1
day
−1
) and samples of the hippocampus were obtained. Assessments of the OS markers, protein carbonyls, and malondialdehyde levels demonstrated their significant increase (∼3 fold) with aging that were partially suppressed by Epi. The protein levels of the glial fibrillary acidic protein, inflammatory factor 1 (Iba1), pro-inflammatory cytokines, interleukins (IL-1β, IL-3, 5, 6 and 15), cyclooxygenase 2, tumor necrosis factor α, nuclear factor-activated B cells and interferon γ increase with aging and were also significantly decreased with Epi treatment. However, anti-inflammatory cytokines, IL-1ra, IL-10 and 11 decrease with aging and were restored with Epi. Epi also reversed the aging effects on the hyperphosphorylation of tau, increased soluble β-amyloid levels (∼2 fold), cellular death (as per caspase 3 and 9 activity), and reduced nerve growth factor and triggering receptor expressed on myeloid cells 2 levels. Measures of anxiety like-behavior and memory demonstrated improvements with Epi treatment. Indicators of systemic inflammation increase with aging and Epi was capable of decreasing blood inflammatory markers. Altogether, the results show a significant capacity of Epi to mitigate hippocampus OS and inflammation leading to improved brain function. Evidence has implicated oxidative stress (OS) and inflammation as drivers of neurodegenerative pathologies. We previously reported on the beneficial effects of (−)-epicatechin (Epi) treatment on aging-induced OS and its capacity to restore modulators of mitochondrial biogenesis in the prefrontal cortex of 26-month-old male mice. In the present study using the same mouse model of aging, we examined the capacity of Epi to mitigate hippocampus OS, inflammation, hyperphosphorylation of tau protein, soluble β-amyloid protein levels, cell survival, memory, anxiety-like behavior levels and systemic inflammation. Mice were subjected to 4 weeks of Epi treatment (1 mg kg −1 day −1 ) and samples of the hippocampus were obtained. Assessments of the OS markers, protein carbonyls, and malondialdehyde levels demonstrated their significant increase (∼3 fold) with aging that were partially suppressed by Epi. The protein levels of the glial fibrillary acidic protein, inflammatory factor 1 (Iba1), pro-inflammatory cytokines, interleukins (IL-1β, IL-3, 5, 6 and 15), cyclooxygenase 2, tumor necrosis factor α, nuclear factor-activated B cells and interferon γ increase with aging and were also significantly decreased with Epi treatment. However, anti-inflammatory cytokines, IL-1ra, IL-10 and 11 decrease with aging and were restored with Epi. Epi also reversed the aging effects on the hyperphosphorylation of tau, increased soluble β-amyloid levels (∼2 fold), cellular death (as per caspase 3 and 9 activity), and reduced nerve growth factor and triggering receptor expressed on myeloid cells 2 levels. Measures of anxiety like-behavior and memory demonstrated improvements with Epi treatment. Indicators of systemic inflammation increase with aging and Epi was capable of decreasing blood inflammatory markers. Altogether, the results show a significant capacity of Epi to mitigate hippocampus OS and inflammation leading to improved brain function. (−)-Epicatechin reduces neuroinflammation and Tau-hp, improving memory and learning. Evidence has implicated oxidative stress (OS) and inflammation as drivers of neurodegenerative pathologies. We previously reported on the beneficial effects of (-)-epicatechin (Epi) treatment on aging-induced OS and its capacity to restore modulators of mitochondrial biogenesis in the prefrontal cortex of 26-month-old male mice. In the present study using the same mouse model of aging, we examined the capacity of Epi to mitigate hippocampus OS, inflammation, hyperphosphorylation of tau protein, soluble β-amyloid protein levels, cell survival, memory, anxiety-like behavior levels and systemic inflammation. Mice were subjected to 4 weeks of Epi treatment (1 mg kg day ) and samples of the hippocampus were obtained. Assessments of the OS markers, protein carbonyls, and malondialdehyde levels demonstrated their significant increase (∼3 fold) with aging that were partially suppressed by Epi. The protein levels of the glial fibrillary acidic protein, inflammatory factor 1 (Iba1), pro-inflammatory cytokines, interleukins (IL-1β, IL-3, 5, 6 and 15), cyclooxygenase 2, tumor necrosis factor α, nuclear factor-activated B cells and interferon γ increase with aging and were also significantly decreased with Epi treatment. However, anti-inflammatory cytokines, IL-1ra, IL-10 and 11 decrease with aging and were restored with Epi. Epi also reversed the aging effects on the hyperphosphorylation of tau, increased soluble β-amyloid levels (∼2 fold), cellular death (as per caspase 3 and 9 activity), and reduced nerve growth factor and triggering receptor expressed on myeloid cells 2 levels. Measures of anxiety like-behavior and memory demonstrated improvements with Epi treatment. Indicators of systemic inflammation increase with aging and Epi was capable of decreasing blood inflammatory markers. Altogether, the results show a significant capacity of Epi to mitigate hippocampus OS and inflammation leading to improved brain function. Evidence has implicated oxidative stress (OS) and inflammation as drivers of neurodegenerative pathologies. We previously reported on the beneficial effects of (−)-epicatechin (Epi) treatment on aging-induced OS and its capacity to restore modulators of mitochondrial biogenesis in the prefrontal cortex of 26-month-old male mice. In the present study using the same mouse model of aging, we examined the capacity of Epi to mitigate hippocampus OS, inflammation, hyperphosphorylation of tau protein, soluble β-amyloid protein levels, cell survival, memory, anxiety-like behavior levels and systemic inflammation. Mice were subjected to 4 weeks of Epi treatment (1 mg kg−1 day−1) and samples of the hippocampus were obtained. Assessments of the OS markers, protein carbonyls, and malondialdehyde levels demonstrated their significant increase (∼3 fold) with aging that were partially suppressed by Epi. The protein levels of the glial fibrillary acidic protein, inflammatory factor 1 (Iba1), pro-inflammatory cytokines, interleukins (IL-1β, IL-3, 5, 6 and 15), cyclooxygenase 2, tumor necrosis factor α, nuclear factor-activated B cells and interferon γ increase with aging and were also significantly decreased with Epi treatment. However, anti-inflammatory cytokines, IL-1ra, IL-10 and 11 decrease with aging and were restored with Epi. Epi also reversed the aging effects on the hyperphosphorylation of tau, increased soluble β-amyloid levels (∼2 fold), cellular death (as per caspase 3 and 9 activity), and reduced nerve growth factor and triggering receptor expressed on myeloid cells 2 levels. Measures of anxiety like-behavior and memory demonstrated improvements with Epi treatment. Indicators of systemic inflammation increase with aging and Epi was capable of decreasing blood inflammatory markers. Altogether, the results show a significant capacity of Epi to mitigate hippocampus OS and inflammation leading to improved brain function. Evidence has implicated oxidative stress (OS) and inflammation as drivers of neurodegenerative pathologies. We previously reported on the beneficial effects of (−)-epicatechin (Epi) treatment, on aging-induced OS and its capacity to restore modulators of mitochondrial biogenesis in the prefrontal cortex of 26-month-old male mice. In the present study using the same mouse model of aging, we examined the capacity of Epi to mitigate hippocampus OS, inflammation, hyperphosphorylation of tau protein, soluble β-amyloid protein levels, cell survival, memory, anxiety-like behavior levels as well as systemic inflammation. Mice underwent 4 weeks of Epi treatment (1 mg/kg/day) and samples of hippocampus were obtained. Assessments of the OS markers protein carbonyls and malondialdehyde levels demonstrated significant increases (~3 fold) with aging that were partially suppressed by Epi. Protein levels of the glial fibrillary acidic protein, inflammatory factor 1 (Iba1), proinflammatory cytokines, interleukins (IL-1β, IL-3, 5, 6 and 15), ciclooxygenase 2, tumor necrosis factor α, nuclear factor activated B cells and interferon γ increase with aging and were also significantly decreased with Epi treatment. However, anti-inflammatory cytokines, IL-1ra, Il-10 and 11 were decreased in aging and were restored with Epi. Epi also reversed aging effects on the hyperphosporylation of tau, increased soluble β-amyloid levels (~2 fold), cell death, (as per caspase 3 and 9 activity), and reductions in nerve growth factor and triggering receptor myeloid cells 2 levels. Measures of anxiety like behavior and memory demonstrated improvements with Epi treatment. Indicators of systemic inflammation were elevated with aging and Epi was capable to decrease blood inflammatory markers. Altogether, results evidence a significant capacity of Epi to mitigate hippocampus OS and inflammation leading to improved brain function. |
Author | Calzada-Mendoza, Claudia Villarreal, Francisco Ramirez-Sanchez, Israel Mendoza-Lorenzo, Patricia Rodriguez, Alonso Navarrete-Yañez, Viridiana Ceballos, Guillermo Hogan, Michael C Garate-Carrillo, Alejandra |
AuthorAffiliation | San Diego Sección de Estudios de Posgrado e Investigación Universidad Juárez Autónoma de Tabasco Instituto Politécnico Nacional VA San Diego Health Care System Department of Medicine Escuela Superior de Medicina School of Medicine University of California División Académica de Ciencias Básicas Unidad Chontalpa |
AuthorAffiliation_xml | – name: School of Medicine – name: Universidad Juárez Autónoma de Tabasco – name: University of California – name: Department of Medicine – name: Unidad Chontalpa – name: Escuela Superior de Medicina – name: VA San Diego Health Care System – name: San Diego – name: Instituto Politécnico Nacional – name: Sección de Estudios de Posgrado e Investigación – name: División Académica de Ciencias Básicas – name: 1 Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, México, D.F – name: 3 División Académica de Ciencias Básicas, Unidad Chontalpa, Universidad Juárez Autónoma de Tabasco, Tabasco México – name: 2 Department of Medicine, School of Medicine, University of California, San Diego, La Jolla California, USA – name: 4 VA San Diego Health Care System, San Diego, California, USA |
Author_xml | – sequence: 1 givenname: Viridiana surname: Navarrete-Yañez fullname: Navarrete-Yañez, Viridiana – sequence: 2 givenname: Alejandra surname: Garate-Carrillo fullname: Garate-Carrillo, Alejandra – sequence: 3 givenname: Alonso surname: Rodriguez fullname: Rodriguez, Alonso – sequence: 4 givenname: Patricia surname: Mendoza-Lorenzo fullname: Mendoza-Lorenzo, Patricia – sequence: 5 givenname: Guillermo surname: Ceballos fullname: Ceballos, Guillermo – sequence: 6 givenname: Claudia surname: Calzada-Mendoza fullname: Calzada-Mendoza, Claudia – sequence: 7 givenname: Michael C surname: Hogan fullname: Hogan, Michael C – sequence: 8 givenname: Francisco surname: Villarreal fullname: Villarreal, Francisco – sequence: 9 givenname: Israel surname: Ramirez-Sanchez fullname: Ramirez-Sanchez, Israel |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33201160$$D View this record in MEDLINE/PubMed |
BookMark | eNpVkc1q3DAUhUVIaH6aTfYJhm7SgNtrSZbtTaDkpykMZNNCd0IjX8UKY8mR7MK8Qdd5xDxJ1cxkkgiEhM53jw6cfbLtvENCjgr4UgBrvrZgPFDO6naL7FHgNBcl_N5-ufNG7JLDGO8hLdY0dVN_ILuMUSgKAXvk4coY1GPMvMlOn_4-fs5xsFqNqDvrMu8yh1Pw1pmF6ns12vSiXJt1ywHD0PmYdlguVkKyGNWUpbmxw6yzw-C16ofp2VzdYZv1VuNHsmPUIuLh-jwgv66vfl7c5LPb7z8uvs1yXQIdcwpliXM0ILBgpRZYlRWnlWjmpgQBhpaF4Ipr0A3jFU8kFaxBUQPUVDHDDsj5yneY5j22Gt0Y1EIOwfYqLKVXVr5XnO3knf8jq4oLwVgy-LQ2CP5hwjjKez8FlzJLyiuoOUuREnW2onTwMQY0mx8KkP8bkpdwffvc0GWCT95m2qAvfSTgeAWEqDfqa8XsH9IemT4 |
CitedBy_id | crossref_primary_10_3389_fphar_2022_1035220 crossref_primary_10_3390_cells10061346 crossref_primary_10_3390_molecules26092565 crossref_primary_10_1089_jmf_2021_0084 crossref_primary_10_3390_ijms23042176 crossref_primary_10_14814_phy2_16020 crossref_primary_10_2174_0929867329666211217100020 crossref_primary_10_1016_j_bbrc_2023_149354 crossref_primary_10_1016_j_crfs_2023_100527 crossref_primary_10_3389_fimmu_2022_1006434 crossref_primary_10_3168_jds_2021_20571 crossref_primary_10_1016_j_arr_2024_102224 crossref_primary_10_3390_antiox11071224 crossref_primary_10_2174_1874609815666220819145845 crossref_primary_10_3389_fnins_2021_697319 crossref_primary_10_3390_ph17040518 crossref_primary_10_1096_fj_202201991R crossref_primary_10_1039_D0FO03084H |
Cites_doi | 10.1016/j.ijdevneu.2007.12.003 10.1523/JNEUROSCI.0914-07.2007 10.1016/0006-291X(90)90497-B 10.1517/14740338.4.3.433 10.1159/000331723 10.1097/00005344-200606001-00017 10.1016/j.bbr.2004.03.010 10.1093/gerona/glu131 10.1016/j.sjbs.2016.11.017 10.3390/nu11040756 10.1177/1479164115620982 10.1016/j.cger.2013.07.002 10.1039/C0FO00100G 10.1093/jn/130.8.2115S 10.1007/s12263-008-0091-4 10.1038/tp.2014.135 10.1001/jama.290.8.1030 10.1371/journal.pone.0042823 10.1016/S0028-3908(01)00019-3 10.3389/fphar.2018.00001 10.1017/S0007114507886375 10.1016/j.physbeh.2011.02.013 10.1016/S0006-2952(03)00534-3 10.1080/07315724.2004.10719361 10.3233/JAD-160663 10.1126/science.1355616 10.1113/jphysiol.2011.209924 10.1007/s11064-006-9166-z 10.1073/pnas.0510168103 10.1016/S0531-5565(03)00005-6 10.1016/j.freeradbiomed.2011.06.017 10.1097/00005344-200606001-00018 10.1124/jpet.111.184762 10.1371/journal.pone.0063535 10.1111/j.1471-4159.2007.05194.x 10.1126/science.1072994 10.1101/lm.1028008 10.1038/nrd1330 10.1016/j.appet.2016.02.010 |
ContentType | Journal Article |
Copyright | Copyright Royal Society of Chemistry 2020 |
Copyright_xml | – notice: Copyright Royal Society of Chemistry 2020 |
DBID | NPM AAYXX CITATION 7T5 7T7 7TO 7U7 8FD C1K FR3 H94 P64 5PM |
DOI | 10.1039/d0fo02438d |
DatabaseName | PubMed CrossRef Immunology Abstracts Industrial and Applied Microbiology Abstracts (Microbiology A) Oncogenes and Growth Factors Abstracts Toxicology Abstracts Technology Research Database Environmental Sciences and Pollution Management Engineering Research Database AIDS and Cancer Research Abstracts Biotechnology and BioEngineering Abstracts PubMed Central (Full Participant titles) |
DatabaseTitle | PubMed CrossRef Oncogenes and Growth Factors Abstracts Technology Research Database Toxicology Abstracts AIDS and Cancer Research Abstracts Immunology Abstracts Engineering Research Database Industrial and Applied Microbiology Abstracts (Microbiology A) Biotechnology and BioEngineering Abstracts Environmental Sciences and Pollution Management |
DatabaseTitleList | CrossRef PubMed Oncogenes and Growth Factors Abstracts |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Diet & Clinical Nutrition |
EISSN | 2042-650X |
EndPage | 1361 |
ExternalDocumentID | 10_1039_D0FO02438D 33201160 d0fo02438d |
Genre | Journal Article |
GrantInformation_xml | – fundername: NIDDK NIH HHS grantid: R01 DK098717 – fundername: NIA NIH HHS grantid: R21 AG047326 |
GroupedDBID | - 0-7 0R 4.4 53G 705 7~J AAEMU AAGNR AAIWI AANOJ ABDVN ABGFH ABRYZ ACGFS ACLDK ACPRK ADMRA ADSRN AENEX AFRAH AFVBQ AGSTE AGSWI ALMA_UNASSIGNED_HOLDINGS ASKNT AUDPV AZFZN BLAPV BSQNT C6K CKLOX EBS ECGLT EE0 EF- HZ H~N J3I JG O-G O9- P2P RCNCU RIG RNS RPMJG RRC RSCEA SKF SKH SKJ SKM SKR SKZ SLC SLF --- -JG 0R~ AAHBH AAJAE AARTK AAWGC AAXHV ABASK ABEMK ABJNI ABPDG ABXOH AEFDR AENGV AESAV AETIL AFLYV AFOGI AGEGJ AGRSR AHGCF AKBGW ANUXI APEMP GGIMP H13 HZ~ NPM RAOCF RVUXY AAYXX CITATION 7T5 7T7 7TO 7U7 8FD C1K FR3 H94 P64 5PM |
ID | FETCH-LOGICAL-c502t-2055ebef06e135c6e75742769bf5060f25164a4c0c93474bef2639e680082a3f3 |
ISSN | 2042-6496 |
IngestDate | Tue Sep 17 21:19:18 EDT 2024 Thu Oct 10 18:19:00 EDT 2024 Fri Aug 23 00:47:30 EDT 2024 Sat Sep 28 08:30:15 EDT 2024 Sat Jan 08 03:48:07 EST 2022 |
IsDoiOpenAccess | false |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 12 |
Language | English |
LinkModel | OpenURL |
MergedId | FETCHMERGED-LOGICAL-c502t-2055ebef06e135c6e75742769bf5060f25164a4c0c93474bef2639e680082a3f3 |
Notes | Co-senior authors |
ORCID | 0000-0002-3251-4909 0000-0003-2155-3934 0000-0001-8581-2283 |
OpenAccessLink | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7746633 |
PMID | 33201160 |
PQID | 2470843757 |
PQPubID | 2047526 |
PageCount | 11 |
ParticipantIDs | crossref_primary_10_1039_D0FO02438D rsc_primary_d0fo02438d pubmedcentral_primary_oai_pubmedcentral_nih_gov_7746633 pubmed_primary_33201160 proquest_journals_2470843757 |
PublicationCentury | 2000 |
PublicationDate | 2020-12-01 |
PublicationDateYYYYMMDD | 2020-12-01 |
PublicationDate_xml | – month: 12 year: 2020 text: 2020-12-01 day: 01 |
PublicationDecade | 2020 |
PublicationPlace | England |
PublicationPlace_xml | – name: England – name: Cambridge |
PublicationTitle | Food & function |
PublicationTitleAlternate | Food Funct |
PublicationYear | 2020 |
Publisher | Royal Society of Chemistry |
Publisher_xml | – name: Royal Society of Chemistry |
References | Glass (D0FO02438D-(cit2)/*[position()=1]) 2010; 140 Stadtman (D0FO02438D-(cit24)/*[position()=1]) 1992; 257 Pappolla (D0FO02438D-(cit30)/*[position()=1]) 1992; 140 Ishisaka (D0FO02438D-(cit34)/*[position()=1]) 2011; 51 Nakajima (D0FO02438D-(cit42)/*[position()=1]) 2011; 28 Eckert (D0FO02438D-(cit4)/*[position()=1]) 2003; 66 Bisson (D0FO02438D-(cit9)/*[position()=1]) 2008; 100 Rendeiro (D0FO02438D-(cit20)/*[position()=1]) 2013; 8 Xu (D0FO02438D-(cit36)/*[position()=1]) 2006; 31 Nogueira (D0FO02438D-(cit23)/*[position()=1]) 2011; 589 Fisher (D0FO02438D-(cit11)/*[position()=1]) 2006; 47 Shin-ichiro (D0FO02438D-(cit29)/*[position()=1]) 1990; 170 Cho (D0FO02438D-(cit32)/*[position()=1]) 2003; 38 Hooper (D0FO02438D-(cit39)/*[position()=1]) 2008; 104 Crichton (D0FO02438D-(cit17)/*[position()=1]) 2016; 100 Heiss (D0FO02438D-(cit14)/*[position()=1]) 2003; 290 Engler (D0FO02438D-(cit13)/*[position()=1]) 2004; 23 Ramírez-Sánchez (D0FO02438D-(cit25)/*[position()=1]) 2016; 13 Balderas (D0FO02438D-(cit28)/*[position()=1]) 2015; 15 Wang (D0FO02438D-(cit45)/*[position()=1]) 2000; 130 Srividhya (D0FO02438D-(cit33)/*[position()=1]) 2008; 26 Hardy (D0FO02438D-(cit38)/*[position()=1]) 2002; 297 Ola (D0FO02438D-(cit43)/*[position()=1]) 2017; 24 Kamphuis (D0FO02438D-(cit8)/*[position()=1]) 2012; 7 Selmi (D0FO02438D-(cit35)/*[position()=1]) 2006; 47 Moreno-Ulloa (D0FO02438D-(cit22)/*[position()=1]) 2015; 70 Van Praag (D0FO02438D-(cit21)/*[position()=1]) 2007; 27 Gilgun-Sherki (D0FO02438D-(cit31)/*[position()=1]) 2001; 40 Terry (D0FO02438D-(cit5)/*[position()=1]) 2008; 23 Field (D0FO02438D-(cit10)/*[position()=1]) 2011; 103 Middlemore-Risher (D0FO02438D-(cit41)/*[position()=1]) 2011; 339 O'Callaghan (D0FO02438D-(cit7)/*[position()=1]) 2005; 4 Bureau (D0FO02438D-(cit37)/*[position()=1]) 2007; 2639 Barnham (D0FO02438D-(cit1)/*[position()=1]) 2004; 3 Schroeter (D0FO02438D-(cit15)/*[position()=1]) 2006; 103 Vauzour (D0FO02438D-(cit16)/*[position()=1]) 2008; 3 Seibenhener (D0FO02438D-(cit27)/*[position()=1]) 2015 Phan (D0FO02438D-(cit40)/*[position()=1]) 2019; 11 Faria (D0FO02438D-(cit18)/*[position()=1]) 2011; 2 Khan (D0FO02438D-(cit44)/*[position()=1]) 2018; 9 Francis (D0FO02438D-(cit12)/*[position()=1]) 2006; 47 Roy (D0FO02438D-(cit26)/*[position()=1]) 2004; 154 Harada (D0FO02438D-(cit3)/*[position()=1]) 2013; 29 Stringer (D0FO02438D-(cit19)/*[position()=1]) 2015; 5 Raha (D0FO02438D-(cit6)/*[position()=1]) 2016; 55 |
References_xml | – volume: 26 start-page: 217 year: 2008 ident: D0FO02438D-(cit33)/*[position()=1] publication-title: Int. J. Dev. Neurosci. doi: 10.1016/j.ijdevneu.2007.12.003 contributor: fullname: Srividhya – volume: 27 start-page: 5869 year: 2007 ident: D0FO02438D-(cit21)/*[position()=1] publication-title: J. Neurosci. doi: 10.1523/JNEUROSCI.0914-07.2007 contributor: fullname: Van Praag – volume: 170 start-page: 1044 year: 1990 ident: D0FO02438D-(cit29)/*[position()=1] publication-title: Biochem. Biophys. Res. Commun. doi: 10.1016/0006-291X(90)90497-B contributor: fullname: Shin-ichiro – volume: 4 start-page: 433 year: 2005 ident: D0FO02438D-(cit7)/*[position()=1] publication-title: Expert Opin. Drug Saf. doi: 10.1517/14740338.4.3.433 contributor: fullname: O'Callaghan – volume: 28 start-page: 147 year: 2011 ident: D0FO02438D-(cit42)/*[position()=1] publication-title: Cell. Physiol. Biochem. doi: 10.1159/000331723 contributor: fullname: Nakajima – volume: 47 start-page: 210 year: 2006 ident: D0FO02438D-(cit11)/*[position()=1] publication-title: J. Cardiovasc. Pharmacol. doi: 10.1097/00005344-200606001-00017 contributor: fullname: Fisher – volume: 154 start-page: 439 year: 2004 ident: D0FO02438D-(cit26)/*[position()=1] publication-title: Behav. Brain Res. doi: 10.1016/j.bbr.2004.03.010 contributor: fullname: Roy – volume: 70 start-page: 1370 year: 2015 ident: D0FO02438D-(cit22)/*[position()=1] publication-title: J. Gerontol., Ser. A doi: 10.1093/gerona/glu131 contributor: fullname: Moreno-Ulloa – volume: 2639 start-page: 2631 year: 2007 ident: D0FO02438D-(cit37)/*[position()=1] publication-title: J. Neurosci. Res. contributor: fullname: Bureau – volume: 24 start-page: 1186 year: 2017 ident: D0FO02438D-(cit43)/*[position()=1] publication-title: Saudi J. Biol. Sci. doi: 10.1016/j.sjbs.2016.11.017 contributor: fullname: Ola – start-page: 52434 year: 2015 ident: D0FO02438D-(cit27)/*[position()=1] publication-title: J. Visualized Exp. contributor: fullname: Seibenhener – volume: 140 start-page: 621 year: 1992 ident: D0FO02438D-(cit30)/*[position()=1] publication-title: Am. J. Pathol. contributor: fullname: Pappolla – volume: 11 start-page: 756 issue: 4 year: 2019 ident: D0FO02438D-(cit40)/*[position()=1] publication-title: Nutrients doi: 10.3390/nu11040756 contributor: fullname: Phan – volume: 13 start-page: 201 year: 2016 ident: D0FO02438D-(cit25)/*[position()=1] publication-title: Diabetes Vasc. Dis. Res. doi: 10.1177/1479164115620982 contributor: fullname: Ramírez-Sánchez – volume: 140 start-page: 918 year: 2010 ident: D0FO02438D-(cit2)/*[position()=1] publication-title: Nih contributor: fullname: Glass – volume: 29 start-page: 737 year: 2013 ident: D0FO02438D-(cit3)/*[position()=1] publication-title: Clin. Geriatr. Med. doi: 10.1016/j.cger.2013.07.002 contributor: fullname: Harada – volume: 2 start-page: 39 year: 2011 ident: D0FO02438D-(cit18)/*[position()=1] publication-title: Food Funct. doi: 10.1039/C0FO00100G contributor: fullname: Faria – volume: 130 start-page: 2115S year: 2000 ident: D0FO02438D-(cit45)/*[position()=1] publication-title: J. Nutr. doi: 10.1093/jn/130.8.2115S contributor: fullname: Wang – volume: 3 start-page: 115 year: 2008 ident: D0FO02438D-(cit16)/*[position()=1] publication-title: Genes Nutr. doi: 10.1007/s12263-008-0091-4 contributor: fullname: Vauzour – volume: 5 start-page: e493 year: 2015 ident: D0FO02438D-(cit19)/*[position()=1] publication-title: Transl. Psychiatry doi: 10.1038/tp.2014.135 contributor: fullname: Stringer – volume: 290 start-page: 1030 year: 2003 ident: D0FO02438D-(cit14)/*[position()=1] publication-title: J. Am. Med. Assoc. doi: 10.1001/jama.290.8.1030 contributor: fullname: Heiss – volume: 7 start-page: 42823 year: 2012 ident: D0FO02438D-(cit8)/*[position()=1] publication-title: PLoS One doi: 10.1371/journal.pone.0042823 contributor: fullname: Kamphuis – volume: 40 start-page: 959 year: 2001 ident: D0FO02438D-(cit31)/*[position()=1] publication-title: Neuropharmacology doi: 10.1016/S0028-3908(01)00019-3 contributor: fullname: Gilgun-Sherki – volume: 9 start-page: 1 year: 2018 ident: D0FO02438D-(cit44)/*[position()=1] publication-title: Front. Pharmacol. doi: 10.3389/fphar.2018.00001 contributor: fullname: Khan – volume: 100 start-page: 94 year: 2008 ident: D0FO02438D-(cit9)/*[position()=1] publication-title: Br. J. Nutr. doi: 10.1017/S0007114507886375 contributor: fullname: Bisson – volume: 103 start-page: 255 year: 2011 ident: D0FO02438D-(cit10)/*[position()=1] publication-title: Physiol. Behav. doi: 10.1016/j.physbeh.2011.02.013 contributor: fullname: Field – volume: 66 start-page: 1627 year: 2003 ident: D0FO02438D-(cit4)/*[position()=1] publication-title: Biochem. Pharmacol. doi: 10.1016/S0006-2952(03)00534-3 contributor: fullname: Eckert – volume: 23 start-page: 197 year: 2004 ident: D0FO02438D-(cit13)/*[position()=1] publication-title: J. Am. Coll. Nutr. doi: 10.1080/07315724.2004.10719361 contributor: fullname: Engler – volume: 55 start-page: 199 year: 2016 ident: D0FO02438D-(cit6)/*[position()=1] publication-title: J. Alzheimer's Dis. doi: 10.3233/JAD-160663 contributor: fullname: Raha – volume: 257 start-page: 1220 year: 1992 ident: D0FO02438D-(cit24)/*[position()=1] publication-title: Science doi: 10.1126/science.1355616 contributor: fullname: Stadtman – volume: 589 start-page: 4615 year: 2011 ident: D0FO02438D-(cit23)/*[position()=1] publication-title: J. Physiol. doi: 10.1113/jphysiol.2011.209924 contributor: fullname: Nogueira – volume: 31 start-page: 1263 year: 2006 ident: D0FO02438D-(cit36)/*[position()=1] publication-title: Neurochem. Res. doi: 10.1007/s11064-006-9166-z contributor: fullname: Xu – volume: 103 start-page: 1024 issue: 4 year: 2006 ident: D0FO02438D-(cit15)/*[position()=1] publication-title: Proc. Natl. Acad. Sci. U. S. A. doi: 10.1073/pnas.0510168103 contributor: fullname: Schroeter – volume: 38 start-page: 539 year: 2003 ident: D0FO02438D-(cit32)/*[position()=1] publication-title: Exp. Gerontol. doi: 10.1016/S0531-5565(03)00005-6 contributor: fullname: Cho – volume: 51 start-page: 1329 year: 2011 ident: D0FO02438D-(cit34)/*[position()=1] publication-title: Free Radicals Biol. Med. doi: 10.1016/j.freeradbiomed.2011.06.017 contributor: fullname: Ishisaka – volume: 47 start-page: 215 year: 2006 ident: D0FO02438D-(cit12)/*[position()=1] publication-title: J. Cardiovasc. Pharmacol. doi: 10.1097/00005344-200606001-00018 contributor: fullname: Francis – volume: 47 start-page: 163 year: 2006 ident: D0FO02438D-(cit35)/*[position()=1] publication-title: Inflammation contributor: fullname: Selmi – volume: 339 start-page: 341 year: 2011 ident: D0FO02438D-(cit41)/*[position()=1] publication-title: J. Pharmacol. Exp. Ther. doi: 10.1124/jpet.111.184762 contributor: fullname: Middlemore-Risher – volume: 8 start-page: 1 year: 2013 ident: D0FO02438D-(cit20)/*[position()=1] publication-title: PLoS One doi: 10.1371/journal.pone.0063535 contributor: fullname: Rendeiro – volume: 104 start-page: 1433 year: 2008 ident: D0FO02438D-(cit39)/*[position()=1] publication-title: J. Neurochem. doi: 10.1111/j.1471-4159.2007.05194.x contributor: fullname: Hooper – volume: 23 start-page: 1 year: 2008 ident: D0FO02438D-(cit5)/*[position()=1] publication-title: Bone contributor: fullname: Terry – volume: 297 start-page: 353 year: 2002 ident: D0FO02438D-(cit38)/*[position()=1] publication-title: Science doi: 10.1126/science.1072994 contributor: fullname: Hardy – volume: 15 start-page: 618 issue: 9 year: 2015 ident: D0FO02438D-(cit28)/*[position()=1] publication-title: Learn Mem. doi: 10.1101/lm.1028008 contributor: fullname: Balderas – volume: 3 start-page: 205 year: 2004 ident: D0FO02438D-(cit1)/*[position()=1] publication-title: Nat. Rev. Drug Discovery doi: 10.1038/nrd1330 contributor: fullname: Barnham – volume: 100 start-page: 126 year: 2016 ident: D0FO02438D-(cit17)/*[position()=1] publication-title: Appetite doi: 10.1016/j.appet.2016.02.010 contributor: fullname: Crichton |
SSID | ssj0000399898 |
Score | 2.394654 |
Snippet | Evidence has implicated oxidative stress (OS) and inflammation as drivers of neurodegenerative pathologies. We previously reported on the beneficial effects of... |
SourceID | pubmedcentral proquest crossref pubmed rsc |
SourceType | Open Access Repository Aggregation Database Index Database Publisher |
StartPage | 1351 |
SubjectTerms | Aging Aging (artificial) Alzheimer's disease Anxiety Carbonyl compounds Carbonyls Caspase-3 Cell death Cell survival Cyclooxygenase-2 Cytokines Epicatechin Glial fibrillary acidic protein Growth factors Hippocampus Inflammation Interferon Interleukin 1 receptor antagonist Interleukin 1 receptors Interleukin 10 Interleukin 3 Lymphocytes B Malondialdehyde Markers Mitochondria Modulators Myeloid cells Nerve growth factor Neuromodulation Oxidative stress Proteins β-Amyloid γ-Interferon |
Title | Effects of (−)-epicatechin on neuroinflammation and hyperphosphorylation of tau in the hippocampus of aged mice |
URI | https://www.ncbi.nlm.nih.gov/pubmed/33201160 https://www.proquest.com/docview/2470843757 https://pubmed.ncbi.nlm.nih.gov/PMC7746633 |
Volume | 11 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Zj9MwELa63RdeENdCYEGWOARCASe2czx2t3uIo0hoF8pTlcOhQd2kZFMk-gt45l_xN_glzDhHU7oPCw-NWsdxXM9nz4xnPEPIIwk4SPxAmAl3mSlAATB9xkMzliIIOTBcFeN557cj5_hUvBrLca_3q-O1tCjDF9HywnMl_0NVKAO64inZf6Bs2ygUwHegL1yBwnC9FI0PVs4YIChqvwXvsW-Ddm-quT7chp6SaA_QYSvhlUD_6qyiNhpMQQmFcc7P4VN8n7XSYxksGv_HaTqfA7s7my_0a2D1iZ-f1f5yq_SeeawhhEyya9gfBd-0J7AyPwVokd-zqv3qD2mRIi5blnCEAciVuQ-109oYNJipL9DHoq3zPo-L9POiamEwgzHNW7SoLM6XgfkmL1S2zCvJGFMPpEF3V8Pueojoxc_GY0OO8Osw2Z0yycZrq7fVRandWYstNJJ2GDv8ruK-b3ANxjHo6pAdvsP4jN5wxRsbf4C_WGbryKhN-NyfrJ7dItu260vZJ9uD13tHH9sNP6iGuTox2WHz35pwudx_uWpgXUDa0Ho2nXe3iiZXjZaJTq6Rq7UyQwcVMq-TnspuEGOYqpI-oXXE2RkdNQkfbpKvNWJpntCnv3_8fNbFKc0zuoFTChigF-EUmwCcUngOcEo7OMU7iFOKOL1FTg8PTvaPzTrphxlJZpcwv6WEhSVhjrK4jBzlSlfYruOHCcbCTEAed0QgIhb5XLgCatogZCvHQ2E24AnfIf0sz9QdQqXyhFQiCmwZisjyQ5C2WeJaInF9N3A8gzxsRnoyr2K7TDYJapDdhgiTeu6fT2zhMk9w6JtBblf0aJvgHIVqhxnEXaNUWwEjuq_fydKpjuwOuhhoANwgO0DTtn7Mklz3Jb57qR7fI1dWU2qX9Mtioe6D6FyGD2pQ_gFxOMSj |
link.rule.ids | 230,315,786,790,891,27955,27956 |
linkProvider | Royal Society of Chemistry |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Effects+of+%28%E2%88%92%29-epicatechin+on+neuroinflammation+and+hyperphosphorylation+of+tau+in+the+hippocampus+of+aged+mice&rft.jtitle=Food+%26+function&rft.au=Navarrete-Ya%C3%B1ez%2C+Viridiana&rft.au=Garate-Carrillo%2C+Alejandra&rft.au=Rodriguez%2C+Alonso&rft.au=Mendoza-Lorenzo%2C+Patricia&rft.date=2020-12-01&rft.issn=2042-6496&rft.eissn=2042-650X&rft.volume=11&rft.issue=12&rft.spage=10351&rft.epage=10361&rft_id=info:doi/10.1039%2FD0FO02438D&rft.externalDBID=n%2Fa&rft.externalDocID=10_1039_D0FO02438D |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2042-6496&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2042-6496&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2042-6496&client=summon |