Emodin protected against synaptic impairment and oxidative stress induced by fluoride in SH‐SY5Y cells by modulating ERK1/2/Nrf2/HO‐1 pathway
Excessive fluoride exposure contributes to neurotoxic effects. Emodin exhibits antioxidative functions in the central nervous system (CNS); however, its neuroprotective mechanism against fluoride remains to be elucidated. Our aim was to explore the neuroprotective efficacy and the possible mechanism...
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| Veröffentlicht in: | Environmental toxicology 2020-09, Vol.35 (9), p.922-929 |
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| creator | Lai, Chencen Chen, Qian Ding, Yuanting Liu, Heng Tang, Zhi |
| description | Excessive fluoride exposure contributes to neurotoxic effects. Emodin exhibits antioxidative functions in the central nervous system (CNS); however, its neuroprotective mechanism against fluoride remains to be elucidated. Our aim was to explore the neuroprotective efficacy and the possible mechanisms of emodin. In our study, synaptic proteins and oxidative stress damage were examined after human neuroblastoma SH‐SY5Y cells were treated with high doses of NaF for 24 hours. Moreover, pretreatment with emodin was used to shed light on the neuroprotective effects in NaF‐induced toxicity in SH‐SY5Y cells. We found that NaF significantly lowered the protein expressions of SNAP 25, synaptophysin and PSD 95 in SH‐SY5Y cells. In addition, NaF exposure increased the protein expression of p‐ERK1/2 and decreased the protein expressions of Nrf2 and HO‐1, as well as facilitated increasing ROS, 4‐hydroxynonenal (4‐HNE), and 8‐Hydroxy‐2′‐deoxyguanosine (8‐OHdG). Pretreatment with emodin significantly recovered these alterations caused by NaF. These data implied that the neuroprotective effects of emodin and pointed to the promising utilization for protecting against neurotoxicity induced by fluoride. |
| doi_str_mv | 10.1002/tox.22928 |
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Emodin exhibits antioxidative functions in the central nervous system (CNS); however, its neuroprotective mechanism against fluoride remains to be elucidated. Our aim was to explore the neuroprotective efficacy and the possible mechanisms of emodin. In our study, synaptic proteins and oxidative stress damage were examined after human neuroblastoma SH‐SY5Y cells were treated with high doses of NaF for 24 hours. Moreover, pretreatment with emodin was used to shed light on the neuroprotective effects in NaF‐induced toxicity in SH‐SY5Y cells. We found that NaF significantly lowered the protein expressions of SNAP 25, synaptophysin and PSD 95 in SH‐SY5Y cells. In addition, NaF exposure increased the protein expression of p‐ERK1/2 and decreased the protein expressions of Nrf2 and HO‐1, as well as facilitated increasing ROS, 4‐hydroxynonenal (4‐HNE), and 8‐Hydroxy‐2′‐deoxyguanosine (8‐OHdG). Pretreatment with emodin significantly recovered these alterations caused by NaF. These data implied that the neuroprotective effects of emodin and pointed to the promising utilization for protecting against neurotoxicity induced by fluoride.</description><identifier>ISSN: 1520-4081</identifier><identifier>EISSN: 1522-7278</identifier><identifier>DOI: 10.1002/tox.22928</identifier><identifier>PMID: 32293791</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>8-Hydroxydeoxyguanosine ; Biological stress ; Cells ; Central nervous system ; Deoxyguanosine ; Emodin ; ERK1/2 ; Extracellular signal-regulated kinase ; fluoride ; Fluorides ; Neuroprotection ; Neurotoxicity ; Nrf2/HO‐1 ; Oxidative stress ; Pretreatment ; Proteins ; synapse ; Synaptophysin ; Toxicity</subject><ispartof>Environmental toxicology, 2020-09, Vol.35 (9), p.922-929</ispartof><rights>2020 Wiley Periodicals, Inc.</rights><rights>2020 Wiley Periodicals LLC</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3908-d584a7f5b9c00a9681d41560b97a41dc9c481ead51904a39030b6f70cbf94a143</citedby><cites>FETCH-LOGICAL-c3908-d584a7f5b9c00a9681d41560b97a41dc9c481ead51904a39030b6f70cbf94a143</cites><orcidid>0000-0002-6506-9290</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Ftox.22928$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Ftox.22928$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27922,27923,45572,45573</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32293791$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lai, Chencen</creatorcontrib><creatorcontrib>Chen, Qian</creatorcontrib><creatorcontrib>Ding, Yuanting</creatorcontrib><creatorcontrib>Liu, Heng</creatorcontrib><creatorcontrib>Tang, Zhi</creatorcontrib><title>Emodin protected against synaptic impairment and oxidative stress induced by fluoride in SH‐SY5Y cells by modulating ERK1/2/Nrf2/HO‐1 pathway</title><title>Environmental toxicology</title><addtitle>Environ Toxicol</addtitle><description>Excessive fluoride exposure contributes to neurotoxic effects. Emodin exhibits antioxidative functions in the central nervous system (CNS); however, its neuroprotective mechanism against fluoride remains to be elucidated. Our aim was to explore the neuroprotective efficacy and the possible mechanisms of emodin. In our study, synaptic proteins and oxidative stress damage were examined after human neuroblastoma SH‐SY5Y cells were treated with high doses of NaF for 24 hours. Moreover, pretreatment with emodin was used to shed light on the neuroprotective effects in NaF‐induced toxicity in SH‐SY5Y cells. We found that NaF significantly lowered the protein expressions of SNAP 25, synaptophysin and PSD 95 in SH‐SY5Y cells. In addition, NaF exposure increased the protein expression of p‐ERK1/2 and decreased the protein expressions of Nrf2 and HO‐1, as well as facilitated increasing ROS, 4‐hydroxynonenal (4‐HNE), and 8‐Hydroxy‐2′‐deoxyguanosine (8‐OHdG). Pretreatment with emodin significantly recovered these alterations caused by NaF. These data implied that the neuroprotective effects of emodin and pointed to the promising utilization for protecting against neurotoxicity induced by fluoride.</description><subject>8-Hydroxydeoxyguanosine</subject><subject>Biological stress</subject><subject>Cells</subject><subject>Central nervous system</subject><subject>Deoxyguanosine</subject><subject>Emodin</subject><subject>ERK1/2</subject><subject>Extracellular signal-regulated kinase</subject><subject>fluoride</subject><subject>Fluorides</subject><subject>Neuroprotection</subject><subject>Neurotoxicity</subject><subject>Nrf2/HO‐1</subject><subject>Oxidative stress</subject><subject>Pretreatment</subject><subject>Proteins</subject><subject>synapse</subject><subject>Synaptophysin</subject><subject>Toxicity</subject><issn>1520-4081</issn><issn>1522-7278</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp1kMtOxCAUhonReF_4AobElYtaoPTC0pjRMU6cRMfEWTUUqGJ6E6gz3fkI-oo-ieioO1cQ-P7_5HwAHGB0ghEioWuXJ4Qwkq2BbRwTEqQkzda_7yigKMNbYMfaJ4QQS-JkE2xFno5ShrfB-6hupW5gZ1qnhFMS8geuG-ugHRreOS2grjuuTa0aB3kjYbvUkjv9oqB1RlkLdSN74YPFAMuqb42Wyr_B2_HH69vtPJ5DoarKfn37UX3ls80DHN1c4ZCE16Yk4XjqSQw77h4XfNgDGyWvrNr_OXfB3flodjYOJtOLy7PTSSAihrJAxhnlaRkXTCDEWZJhSXGcoIKlnGIpmKAZVlzGmCHKfSRCRVKmSBQloxzTaBccrXr96s-9si5_anvT-JE5oZFXhUmSeOp4RQnTWmtUmXdG19wMOUb5l_zcy8-_5Xv28KexL2ol_8hf2x4IV8BCV2r4vymfTe9XlZ-UjpBQ</recordid><startdate>202009</startdate><enddate>202009</enddate><creator>Lai, Chencen</creator><creator>Chen, Qian</creator><creator>Ding, Yuanting</creator><creator>Liu, Heng</creator><creator>Tang, Zhi</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QH</scope><scope>7ST</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>C1K</scope><scope>F1W</scope><scope>H97</scope><scope>K9.</scope><scope>L.G</scope><scope>M7N</scope><scope>SOI</scope><orcidid>https://orcid.org/0000-0002-6506-9290</orcidid></search><sort><creationdate>202009</creationdate><title>Emodin protected against synaptic impairment and oxidative stress induced by fluoride in SH‐SY5Y cells by modulating ERK1/2/Nrf2/HO‐1 pathway</title><author>Lai, Chencen ; Chen, Qian ; Ding, Yuanting ; Liu, Heng ; Tang, Zhi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3908-d584a7f5b9c00a9681d41560b97a41dc9c481ead51904a39030b6f70cbf94a143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>8-Hydroxydeoxyguanosine</topic><topic>Biological stress</topic><topic>Cells</topic><topic>Central nervous system</topic><topic>Deoxyguanosine</topic><topic>Emodin</topic><topic>ERK1/2</topic><topic>Extracellular signal-regulated kinase</topic><topic>fluoride</topic><topic>Fluorides</topic><topic>Neuroprotection</topic><topic>Neurotoxicity</topic><topic>Nrf2/HO‐1</topic><topic>Oxidative stress</topic><topic>Pretreatment</topic><topic>Proteins</topic><topic>synapse</topic><topic>Synaptophysin</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lai, Chencen</creatorcontrib><creatorcontrib>Chen, Qian</creatorcontrib><creatorcontrib>Ding, Yuanting</creatorcontrib><creatorcontrib>Liu, Heng</creatorcontrib><creatorcontrib>Tang, Zhi</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Aqualine</collection><collection>Environment Abstracts</collection><collection>Oceanic Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Water Resources Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Environment Abstracts</collection><jtitle>Environmental toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lai, Chencen</au><au>Chen, Qian</au><au>Ding, Yuanting</au><au>Liu, Heng</au><au>Tang, Zhi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Emodin protected against synaptic impairment and oxidative stress induced by fluoride in SH‐SY5Y cells by modulating ERK1/2/Nrf2/HO‐1 pathway</atitle><jtitle>Environmental toxicology</jtitle><addtitle>Environ Toxicol</addtitle><date>2020-09</date><risdate>2020</risdate><volume>35</volume><issue>9</issue><spage>922</spage><epage>929</epage><pages>922-929</pages><issn>1520-4081</issn><eissn>1522-7278</eissn><abstract>Excessive fluoride exposure contributes to neurotoxic effects. Emodin exhibits antioxidative functions in the central nervous system (CNS); however, its neuroprotective mechanism against fluoride remains to be elucidated. Our aim was to explore the neuroprotective efficacy and the possible mechanisms of emodin. In our study, synaptic proteins and oxidative stress damage were examined after human neuroblastoma SH‐SY5Y cells were treated with high doses of NaF for 24 hours. Moreover, pretreatment with emodin was used to shed light on the neuroprotective effects in NaF‐induced toxicity in SH‐SY5Y cells. We found that NaF significantly lowered the protein expressions of SNAP 25, synaptophysin and PSD 95 in SH‐SY5Y cells. In addition, NaF exposure increased the protein expression of p‐ERK1/2 and decreased the protein expressions of Nrf2 and HO‐1, as well as facilitated increasing ROS, 4‐hydroxynonenal (4‐HNE), and 8‐Hydroxy‐2′‐deoxyguanosine (8‐OHdG). Pretreatment with emodin significantly recovered these alterations caused by NaF. These data implied that the neuroprotective effects of emodin and pointed to the promising utilization for protecting against neurotoxicity induced by fluoride.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>32293791</pmid><doi>10.1002/tox.22928</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-6506-9290</orcidid></addata></record> |
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| subjects | 8-Hydroxydeoxyguanosine Biological stress Cells Central nervous system Deoxyguanosine Emodin ERK1/2 Extracellular signal-regulated kinase fluoride Fluorides Neuroprotection Neurotoxicity Nrf2/HO‐1 Oxidative stress Pretreatment Proteins synapse Synaptophysin Toxicity |
| title | Emodin protected against synaptic impairment and oxidative stress induced by fluoride in SH‐SY5Y cells by modulating ERK1/2/Nrf2/HO‐1 pathway |
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