Gastrodin ameliorates synaptic impairment, mitochondrial dysfunction and oxidative stress in N2a/APP cells
Alzheimer's disease is characterized by abnormal β-amyloid and tau accumulation, mitochondrial dysfunction, oxidative stress, and synaptic dysfunction. Here, we aimed to assess the mechanisms and signalling pathways in the neuroprotective effect of gastrodin, a phenolic glycoside, on murine neu...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2024-07, Vol.719, p.150127, Article 150127 |
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| creator | Tang, Zhi Peng, Yaqian Jiang, Yi Wang, Li Guo, Min Chen, Zhuyi Luo, Chao Zhang, Ting Xiao, Yan Ni, Ruiqing Qi, Xiaolan |
| description | Alzheimer's disease is characterized by abnormal β-amyloid and tau accumulation, mitochondrial dysfunction, oxidative stress, and synaptic dysfunction. Here, we aimed to assess the mechanisms and signalling pathways in the neuroprotective effect of gastrodin, a phenolic glycoside, on murine neuroblastoma N2a cells expressing human Swedish mutant APP (N2a/APP). We found that gastrodin increased the levels of presynaptic-SNAP, synaptophysin, and postsynaptic-PSD95 and reduced phospho-tau Ser396, APP and Aβ1-42 levels in N2a/APP cells. Gastrodin treatment reduced reactive oxygen species generation, lipid peroxidation, mitochondrial fragmentation and DNA oxidation; restored mitochondrial membrane potential and intracellular ATP production. Upregulated phospho-GSK-3β and reduced phospho-ERK and phospho-JNK were involved in the protective effect of gastrodin. In conclusion, we demonstrated the neuroprotective effect of gastrodin in the N2a/APP cell line by ameliorating the impairment on synaptic and mitochondrial function, reducing tau phosphorylation, Aβ1-42 levels as well as reactive oxygen species generation. These results provide new mechanistic insights into the potential effect of gastrodin in the treatment of Alzheimer's disease.
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•Gastrodin is neuroprotective in the N2a/APP cell model of Alzheimer's disease.•Effects of gastrodin involve the ERK1/2, GSK-3β and JNK signalling pathways.•Gastrodin ameliorates synaptic, mitochrondrial, ROS damages, modulates APP processing, and tau phosphorylation in N2a/APP cell. |
| doi_str_mv | 10.1016/j.bbrc.2024.150127 |
| format | Article |
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[Display omitted]
•Gastrodin is neuroprotective in the N2a/APP cell model of Alzheimer's disease.•Effects of gastrodin involve the ERK1/2, GSK-3β and JNK signalling pathways.•Gastrodin ameliorates synaptic, mitochrondrial, ROS damages, modulates APP processing, and tau phosphorylation in N2a/APP cell.</description><identifier>ISSN: 0006-291X</identifier><identifier>ISSN: 1090-2104</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2024.150127</identifier><identifier>PMID: 38761634</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Alzheimer disease ; Alzheimer Disease - drug therapy ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Amyloid beta-Peptides - metabolism ; Amyloid beta-Protein Precursor - genetics ; Amyloid beta-Protein Precursor - metabolism ; Amyloid precursor protein ; Animals ; Benzyl Alcohols - pharmacology ; Cell Line, Tumor ; cell lines ; DNA ; ERK1/2 ; Gastrodin ; Glucosides - pharmacology ; glycosides ; GSK-3β ; Humans ; JNK ; lipid peroxidation ; membrane potential ; Membrane Potential, Mitochondrial - drug effects ; Mice ; mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitochondrial ; mitochondrial membrane ; mutants ; Neuroprotective Agents - pharmacology ; neuroprotective effect ; oxidation ; Oxidative stress ; Oxidative Stress - drug effects ; Peptide Fragments ; phosphorylation ; reactive oxygen species ; Reactive Oxygen Species - metabolism ; Synapses - drug effects ; Synapses - metabolism ; Tau ; tau Proteins - metabolism</subject><ispartof>Biochemical and biophysical research communications, 2024-07, Vol.719, p.150127, Article 150127</ispartof><rights>2024 The Author(s)</rights><rights>Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c433t-9aee599bd0cafcd21ce1b67af2100e1b329a0ec6195ca51a18ad2d1c0dc248c23</citedby><cites>FETCH-LOGICAL-c433t-9aee599bd0cafcd21ce1b67af2100e1b329a0ec6195ca51a18ad2d1c0dc248c23</cites><orcidid>0000-0002-6506-9290 ; 0000-0002-0793-2113</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X24006636$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38761634$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tang, Zhi</creatorcontrib><creatorcontrib>Peng, Yaqian</creatorcontrib><creatorcontrib>Jiang, Yi</creatorcontrib><creatorcontrib>Wang, Li</creatorcontrib><creatorcontrib>Guo, Min</creatorcontrib><creatorcontrib>Chen, Zhuyi</creatorcontrib><creatorcontrib>Luo, Chao</creatorcontrib><creatorcontrib>Zhang, Ting</creatorcontrib><creatorcontrib>Xiao, Yan</creatorcontrib><creatorcontrib>Ni, Ruiqing</creatorcontrib><creatorcontrib>Qi, Xiaolan</creatorcontrib><title>Gastrodin ameliorates synaptic impairment, mitochondrial dysfunction and oxidative stress in N2a/APP cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Alzheimer's disease is characterized by abnormal β-amyloid and tau accumulation, mitochondrial dysfunction, oxidative stress, and synaptic dysfunction. Here, we aimed to assess the mechanisms and signalling pathways in the neuroprotective effect of gastrodin, a phenolic glycoside, on murine neuroblastoma N2a cells expressing human Swedish mutant APP (N2a/APP). We found that gastrodin increased the levels of presynaptic-SNAP, synaptophysin, and postsynaptic-PSD95 and reduced phospho-tau Ser396, APP and Aβ1-42 levels in N2a/APP cells. Gastrodin treatment reduced reactive oxygen species generation, lipid peroxidation, mitochondrial fragmentation and DNA oxidation; restored mitochondrial membrane potential and intracellular ATP production. Upregulated phospho-GSK-3β and reduced phospho-ERK and phospho-JNK were involved in the protective effect of gastrodin. In conclusion, we demonstrated the neuroprotective effect of gastrodin in the N2a/APP cell line by ameliorating the impairment on synaptic and mitochondrial function, reducing tau phosphorylation, Aβ1-42 levels as well as reactive oxygen species generation. These results provide new mechanistic insights into the potential effect of gastrodin in the treatment of Alzheimer's disease.
[Display omitted]
•Gastrodin is neuroprotective in the N2a/APP cell model of Alzheimer's disease.•Effects of gastrodin involve the ERK1/2, GSK-3β and JNK signalling pathways.•Gastrodin ameliorates synaptic, mitochrondrial, ROS damages, modulates APP processing, and tau phosphorylation in N2a/APP cell.</description><subject>Alzheimer disease</subject><subject>Alzheimer Disease - drug therapy</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Amyloid beta-Protein Precursor - genetics</subject><subject>Amyloid beta-Protein Precursor - metabolism</subject><subject>Amyloid precursor protein</subject><subject>Animals</subject><subject>Benzyl Alcohols - pharmacology</subject><subject>Cell Line, Tumor</subject><subject>cell lines</subject><subject>DNA</subject><subject>ERK1/2</subject><subject>Gastrodin</subject><subject>Glucosides - pharmacology</subject><subject>glycosides</subject><subject>GSK-3β</subject><subject>Humans</subject><subject>JNK</subject><subject>lipid peroxidation</subject><subject>membrane potential</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mice</subject><subject>mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondrial</subject><subject>mitochondrial membrane</subject><subject>mutants</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>neuroprotective effect</subject><subject>oxidation</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Peptide Fragments</subject><subject>phosphorylation</subject><subject>reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Synapses - drug effects</subject><subject>Synapses - metabolism</subject><subject>Tau</subject><subject>tau Proteins - metabolism</subject><issn>0006-291X</issn><issn>1090-2104</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFu1DAQhi1ERZfCC3BAOXIgW4-TOGuJS1WVFqlqewCJmzUZT4RXSbzY3op9exJt4diePIfv_zSeX4gPINcgQZ9v110Xaa2kqtfQSFDtK7ECaWSpQNavxUpKqUtl4OepeJvSVkqAWps34rTatBp0Va_E9hpTjsH5qcCRBx8iZk5FOky4y54KP-7Qx5Gn_LkYfQ70K0wuehwKd0j9fqLswxydXBH-eIfZP3IxCzmlYlbeKTy_eHgoiIchvRMnPQ6J3z-9Z-LH16vvlzfl7f31t8uL25LqqsqlQebGmM5Jwp6cAmLodIv9_Ck5j5UyKJk0mIawAYQNOuWApCNVb0hVZ-LT0buL4feeU7ajT8sGOHHYJ1tBU7Vt27TmZVQ2WusamgVVR5RiSClyb3fRjxgPFqRd6rBbu9RhlzrssY459PHJv-9Gdv8j_-4_A1-OAM8HefQcbSLPE7HzkSlbF_xz_r8ZcZ0u</recordid><startdate>20240730</startdate><enddate>20240730</enddate><creator>Tang, Zhi</creator><creator>Peng, Yaqian</creator><creator>Jiang, Yi</creator><creator>Wang, Li</creator><creator>Guo, Min</creator><creator>Chen, Zhuyi</creator><creator>Luo, Chao</creator><creator>Zhang, Ting</creator><creator>Xiao, Yan</creator><creator>Ni, Ruiqing</creator><creator>Qi, Xiaolan</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><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><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0002-6506-9290</orcidid><orcidid>https://orcid.org/0000-0002-0793-2113</orcidid></search><sort><creationdate>20240730</creationdate><title>Gastrodin ameliorates synaptic impairment, mitochondrial dysfunction and oxidative stress in N2a/APP cells</title><author>Tang, Zhi ; Peng, Yaqian ; Jiang, Yi ; Wang, Li ; Guo, Min ; Chen, Zhuyi ; Luo, Chao ; Zhang, Ting ; Xiao, Yan ; Ni, Ruiqing ; Qi, Xiaolan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c433t-9aee599bd0cafcd21ce1b67af2100e1b329a0ec6195ca51a18ad2d1c0dc248c23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Alzheimer disease</topic><topic>Alzheimer Disease - drug therapy</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Amyloid beta-Protein Precursor - genetics</topic><topic>Amyloid beta-Protein Precursor - metabolism</topic><topic>Amyloid precursor protein</topic><topic>Animals</topic><topic>Benzyl Alcohols - pharmacology</topic><topic>Cell Line, Tumor</topic><topic>cell lines</topic><topic>DNA</topic><topic>ERK1/2</topic><topic>Gastrodin</topic><topic>Glucosides - pharmacology</topic><topic>glycosides</topic><topic>GSK-3β</topic><topic>Humans</topic><topic>JNK</topic><topic>lipid peroxidation</topic><topic>membrane potential</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Mice</topic><topic>mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondrial</topic><topic>mitochondrial membrane</topic><topic>mutants</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>neuroprotective effect</topic><topic>oxidation</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Peptide Fragments</topic><topic>phosphorylation</topic><topic>reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Synapses - drug effects</topic><topic>Synapses - metabolism</topic><topic>Tau</topic><topic>tau Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tang, Zhi</creatorcontrib><creatorcontrib>Peng, Yaqian</creatorcontrib><creatorcontrib>Jiang, Yi</creatorcontrib><creatorcontrib>Wang, Li</creatorcontrib><creatorcontrib>Guo, Min</creatorcontrib><creatorcontrib>Chen, Zhuyi</creatorcontrib><creatorcontrib>Luo, Chao</creatorcontrib><creatorcontrib>Zhang, Ting</creatorcontrib><creatorcontrib>Xiao, Yan</creatorcontrib><creatorcontrib>Ni, Ruiqing</creatorcontrib><creatorcontrib>Qi, Xiaolan</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tang, Zhi</au><au>Peng, Yaqian</au><au>Jiang, Yi</au><au>Wang, Li</au><au>Guo, Min</au><au>Chen, Zhuyi</au><au>Luo, Chao</au><au>Zhang, Ting</au><au>Xiao, Yan</au><au>Ni, Ruiqing</au><au>Qi, Xiaolan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gastrodin ameliorates synaptic impairment, mitochondrial dysfunction and oxidative stress in N2a/APP cells</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2024-07-30</date><risdate>2024</risdate><volume>719</volume><spage>150127</spage><pages>150127-</pages><artnum>150127</artnum><issn>0006-291X</issn><issn>1090-2104</issn><eissn>1090-2104</eissn><abstract>Alzheimer's disease is characterized by abnormal β-amyloid and tau accumulation, mitochondrial dysfunction, oxidative stress, and synaptic dysfunction. Here, we aimed to assess the mechanisms and signalling pathways in the neuroprotective effect of gastrodin, a phenolic glycoside, on murine neuroblastoma N2a cells expressing human Swedish mutant APP (N2a/APP). We found that gastrodin increased the levels of presynaptic-SNAP, synaptophysin, and postsynaptic-PSD95 and reduced phospho-tau Ser396, APP and Aβ1-42 levels in N2a/APP cells. Gastrodin treatment reduced reactive oxygen species generation, lipid peroxidation, mitochondrial fragmentation and DNA oxidation; restored mitochondrial membrane potential and intracellular ATP production. Upregulated phospho-GSK-3β and reduced phospho-ERK and phospho-JNK were involved in the protective effect of gastrodin. In conclusion, we demonstrated the neuroprotective effect of gastrodin in the N2a/APP cell line by ameliorating the impairment on synaptic and mitochondrial function, reducing tau phosphorylation, Aβ1-42 levels as well as reactive oxygen species generation. These results provide new mechanistic insights into the potential effect of gastrodin in the treatment of Alzheimer's disease.
[Display omitted]
•Gastrodin is neuroprotective in the N2a/APP cell model of Alzheimer's disease.•Effects of gastrodin involve the ERK1/2, GSK-3β and JNK signalling pathways.•Gastrodin ameliorates synaptic, mitochrondrial, ROS damages, modulates APP processing, and tau phosphorylation in N2a/APP cell.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>38761634</pmid><doi>10.1016/j.bbrc.2024.150127</doi><orcidid>https://orcid.org/0000-0002-6506-9290</orcidid><orcidid>https://orcid.org/0000-0002-0793-2113</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Alzheimer disease Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer Disease - pathology Amyloid beta-Peptides - metabolism Amyloid beta-Protein Precursor - genetics Amyloid beta-Protein Precursor - metabolism Amyloid precursor protein Animals Benzyl Alcohols - pharmacology Cell Line, Tumor cell lines DNA ERK1/2 Gastrodin Glucosides - pharmacology glycosides GSK-3β Humans JNK lipid peroxidation membrane potential Membrane Potential, Mitochondrial - drug effects Mice mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitochondrial mitochondrial membrane mutants Neuroprotective Agents - pharmacology neuroprotective effect oxidation Oxidative stress Oxidative Stress - drug effects Peptide Fragments phosphorylation reactive oxygen species Reactive Oxygen Species - metabolism Synapses - drug effects Synapses - metabolism Tau tau Proteins - metabolism |
| title | Gastrodin ameliorates synaptic impairment, mitochondrial dysfunction and oxidative stress in N2a/APP cells |
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