Neuroprotective Effects of Baicalein on Acrolein-induced Neurotoxicity in the Nigrostriatal Dopaminergic System of Rat Brain
Elevated levels of acrolein, an α,β-unsaturated aldehyde are detected in the brain of patients with Parkinson’s disease (PD). In the present study, the neuroprotective effect of baicalein (a phenolic flavonoid in the dried root of Scutellaria baicalensis Georgi) on acrolein-induced neurodegeneration...
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| Veröffentlicht in: | Molecular neurobiology 2018, Vol.55 (1), p.130-137 |
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| description | Elevated levels of acrolein, an α,β-unsaturated aldehyde are detected in the brain of patients with Parkinson’s disease (PD). In the present study, the neuroprotective effect of baicalein (a phenolic flavonoid in the dried root of
Scutellaria baicalensis
Georgi) on acrolein-induced neurodegeneration of nigrostriatal dopaminergic system was investigated using local infusion of acrolein in the substantia nigra (SN) of rat brain. Systemic administration of baicalein (30 mg/kg, i.p.) significantly attenuated acrolein-induced elevations in 4-hydroxy-2-noneal (a product of lipid peroxidation), N-(3-formyl-3,4-dehydropiperidino)lysine (a biomarker of acrolein-conjugated proteins), and heme-oxygenase-1 levels (a redox-regulated protein) in the infused SN, indicating that baicalein inhibited acrolein-induced oxidative stress and protein conjugation. Furthermore, baicalein reduced acrolein-induced elevations in glial fibrillary acidic protein (a biomarker of activated astrocytes), ED-1 (a biomarker of activated microglia), and mature cathepsin B levels (a cysteine lysosomal protease), suggesting that baicalein attenuated acrolein-induced neuroinflammation. Moreover, baicalein attenuated acrolein-induced caspase 1 activation (a pro-inflammatory caspase) and interleukin-1β levels, indicating that baicalein prevented acrolein-induced inflammasome activation. In addition, baicalein significantly attenuated acrolein-induced caspase 3 activation (a biomarker of apoptosis) as well as acrolein-induced elevation in receptor interacting protein kinase (RIPK) 3 levels (an initiator of necroptosis), indicating that baicalein attenuated apoptosis and necroptosis. At the same time, baicalein mitigated acrolein-induced reduction in dopamine levels in the striatum ipsilateral to acrolein-infused SN. In conclusion, our data suggest that baicalein is neuroprotective via inhibiting oxidative stress, protein conjugation, and inflammation. Furthermore, baicalein prevents acrolein-induced program cell deaths, suggesting that baicalein is therapeutically useful for slowing PD progression. |
| doi_str_mv | 10.1007/s12035-017-0725-x |
| format | Article |
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Scutellaria baicalensis
Georgi) on acrolein-induced neurodegeneration of nigrostriatal dopaminergic system was investigated using local infusion of acrolein in the substantia nigra (SN) of rat brain. Systemic administration of baicalein (30 mg/kg, i.p.) significantly attenuated acrolein-induced elevations in 4-hydroxy-2-noneal (a product of lipid peroxidation), N-(3-formyl-3,4-dehydropiperidino)lysine (a biomarker of acrolein-conjugated proteins), and heme-oxygenase-1 levels (a redox-regulated protein) in the infused SN, indicating that baicalein inhibited acrolein-induced oxidative stress and protein conjugation. Furthermore, baicalein reduced acrolein-induced elevations in glial fibrillary acidic protein (a biomarker of activated astrocytes), ED-1 (a biomarker of activated microglia), and mature cathepsin B levels (a cysteine lysosomal protease), suggesting that baicalein attenuated acrolein-induced neuroinflammation. Moreover, baicalein attenuated acrolein-induced caspase 1 activation (a pro-inflammatory caspase) and interleukin-1β levels, indicating that baicalein prevented acrolein-induced inflammasome activation. In addition, baicalein significantly attenuated acrolein-induced caspase 3 activation (a biomarker of apoptosis) as well as acrolein-induced elevation in receptor interacting protein kinase (RIPK) 3 levels (an initiator of necroptosis), indicating that baicalein attenuated apoptosis and necroptosis. At the same time, baicalein mitigated acrolein-induced reduction in dopamine levels in the striatum ipsilateral to acrolein-infused SN. In conclusion, our data suggest that baicalein is neuroprotective via inhibiting oxidative stress, protein conjugation, and inflammation. Furthermore, baicalein prevents acrolein-induced program cell deaths, suggesting that baicalein is therapeutically useful for slowing PD progression.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-017-0725-x</identifier><identifier>PMID: 28866823</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Acrolein ; Acrolein - toxicity ; Animals ; Antioxidants - pharmacology ; Apoptosis ; Astrocytes ; Biomarkers ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Caspase ; Caspase-1 ; Caspase-3 ; Cathepsin B ; Cell Biology ; Corpus Striatum - drug effects ; Corpus Striatum - metabolism ; Dopamine receptors ; Dopaminergic Neurons - drug effects ; Dopaminergic Neurons - metabolism ; Flavanones - pharmacology ; Glial fibrillary acidic protein ; Heme ; Inflammasomes ; Inflammation ; Kinases ; Lipid peroxidation ; Lysine ; Male ; Microglia ; Movement disorders ; Necroptosis ; Neostriatum ; Neurobiology ; Neurodegeneration ; Neurodegenerative diseases ; Neurology ; Neuroprotection ; Neuroprotective Agents - pharmacology ; Neurosciences ; Neurotoxicity ; Oxidative stress ; Oxygenase ; Parkinson's disease ; Peroxidation ; Phenols ; Protein kinase ; Proteins ; Rats ; Rats, Sprague-Dawley ; Rodents ; Substantia Nigra - drug effects ; Substantia Nigra - metabolism</subject><ispartof>Molecular neurobiology, 2018, Vol.55 (1), p.130-137</ispartof><rights>Springer Science+Business Media, LLC 2017</rights><rights>Molecular Neurobiology is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-508aa0d377b745acb0d528558f8b34a8d5c04e1685ae02bc7b50d68d328045b53</citedby><cites>FETCH-LOGICAL-c442t-508aa0d377b745acb0d528558f8b34a8d5c04e1685ae02bc7b50d68d328045b53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-017-0725-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-017-0725-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28866823$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Wei-Zhong</creatorcontrib><creatorcontrib>Wang, Hsiang-Tsui</creatorcontrib><creatorcontrib>Huang, Hui-Ju</creatorcontrib><creatorcontrib>Lo, Yu-Li</creatorcontrib><creatorcontrib>Lin, Anya Maan-Yuh</creatorcontrib><title>Neuroprotective Effects of Baicalein on Acrolein-induced Neurotoxicity in the Nigrostriatal Dopaminergic System of Rat Brain</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Elevated levels of acrolein, an α,β-unsaturated aldehyde are detected in the brain of patients with Parkinson’s disease (PD). In the present study, the neuroprotective effect of baicalein (a phenolic flavonoid in the dried root of
Scutellaria baicalensis
Georgi) on acrolein-induced neurodegeneration of nigrostriatal dopaminergic system was investigated using local infusion of acrolein in the substantia nigra (SN) of rat brain. Systemic administration of baicalein (30 mg/kg, i.p.) significantly attenuated acrolein-induced elevations in 4-hydroxy-2-noneal (a product of lipid peroxidation), N-(3-formyl-3,4-dehydropiperidino)lysine (a biomarker of acrolein-conjugated proteins), and heme-oxygenase-1 levels (a redox-regulated protein) in the infused SN, indicating that baicalein inhibited acrolein-induced oxidative stress and protein conjugation. Furthermore, baicalein reduced acrolein-induced elevations in glial fibrillary acidic protein (a biomarker of activated astrocytes), ED-1 (a biomarker of activated microglia), and mature cathepsin B levels (a cysteine lysosomal protease), suggesting that baicalein attenuated acrolein-induced neuroinflammation. Moreover, baicalein attenuated acrolein-induced caspase 1 activation (a pro-inflammatory caspase) and interleukin-1β levels, indicating that baicalein prevented acrolein-induced inflammasome activation. In addition, baicalein significantly attenuated acrolein-induced caspase 3 activation (a biomarker of apoptosis) as well as acrolein-induced elevation in receptor interacting protein kinase (RIPK) 3 levels (an initiator of necroptosis), indicating that baicalein attenuated apoptosis and necroptosis. At the same time, baicalein mitigated acrolein-induced reduction in dopamine levels in the striatum ipsilateral to acrolein-infused SN. In conclusion, our data suggest that baicalein is neuroprotective via inhibiting oxidative stress, protein conjugation, and inflammation. Furthermore, baicalein prevents acrolein-induced program cell deaths, suggesting that baicalein is therapeutically useful for slowing PD progression.</description><subject>Acrolein</subject><subject>Acrolein - toxicity</subject><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis</subject><subject>Astrocytes</subject><subject>Biomarkers</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Caspase</subject><subject>Caspase-1</subject><subject>Caspase-3</subject><subject>Cathepsin B</subject><subject>Cell Biology</subject><subject>Corpus Striatum - drug effects</subject><subject>Corpus Striatum - metabolism</subject><subject>Dopamine receptors</subject><subject>Dopaminergic Neurons - drug effects</subject><subject>Dopaminergic Neurons - metabolism</subject><subject>Flavanones - pharmacology</subject><subject>Glial fibrillary acidic protein</subject><subject>Heme</subject><subject>Inflammasomes</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Lipid peroxidation</subject><subject>Lysine</subject><subject>Male</subject><subject>Microglia</subject><subject>Movement disorders</subject><subject>Necroptosis</subject><subject>Neostriatum</subject><subject>Neurobiology</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neurosciences</subject><subject>Neurotoxicity</subject><subject>Oxidative stress</subject><subject>Oxygenase</subject><subject>Parkinson's disease</subject><subject>Peroxidation</subject><subject>Phenols</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Substantia Nigra - drug effects</subject><subject>Substantia Nigra - metabolism</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kMtOAyEUhonR2Hp5ADeGxDV6YIaBLr1rYjTxsiYMw1RMO1RgTJv48FJbdeWKk_D9_8n5EDqgcEwBxEmkDApOgAoCgnEy30BDyvmIUCrZJhqCHBVEVKUcoJ0Y3wAYoyC20YBJWVWSFUP0eW_74GfBJ2uS-7D4sm3zFLFv8Zl2Rk-s67Dv8KkJfjkT1zW9sQ3-DiY_d8alBc5QerX43o2Djyk4nfQEX_iZnrrOhrEz-GkRk50uex91wmdBu24PbbV6Eu3--t1FL1eXz-c35O7h-vb89I6YsmSJcJBaQ1MIUYuSa1NDw5nkXLayLkotG26gtLSSXFtgtRE1h6aSTcEklLzmxS46WvXmO997G5N6833o8krFIItkVTlimaIrKl8aY7CtmgU31WGhKKilb7XyrbJvtfSt5jlzuG7u66ltfhM_gjPAVkDMX93Yhr_V_7d-AYk9jM4</recordid><startdate>2018</startdate><enddate>2018</enddate><creator>Zhao, Wei-Zhong</creator><creator>Wang, Hsiang-Tsui</creator><creator>Huang, Hui-Ju</creator><creator>Lo, Yu-Li</creator><creator>Lin, Anya Maan-Yuh</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>Q9U</scope></search><sort><creationdate>2018</creationdate><title>Neuroprotective Effects of Baicalein on Acrolein-induced Neurotoxicity in the Nigrostriatal Dopaminergic System of Rat Brain</title><author>Zhao, Wei-Zhong ; Wang, Hsiang-Tsui ; Huang, Hui-Ju ; Lo, Yu-Li ; Lin, Anya Maan-Yuh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-508aa0d377b745acb0d528558f8b34a8d5c04e1685ae02bc7b50d68d328045b53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acrolein</topic><topic>Acrolein - toxicity</topic><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Apoptosis</topic><topic>Astrocytes</topic><topic>Biomarkers</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain</topic><topic>Caspase</topic><topic>Caspase-1</topic><topic>Caspase-3</topic><topic>Cathepsin B</topic><topic>Cell Biology</topic><topic>Corpus Striatum - drug effects</topic><topic>Corpus Striatum - metabolism</topic><topic>Dopamine receptors</topic><topic>Dopaminergic Neurons - drug effects</topic><topic>Dopaminergic Neurons - metabolism</topic><topic>Flavanones - pharmacology</topic><topic>Glial fibrillary acidic protein</topic><topic>Heme</topic><topic>Inflammasomes</topic><topic>Inflammation</topic><topic>Kinases</topic><topic>Lipid peroxidation</topic><topic>Lysine</topic><topic>Male</topic><topic>Microglia</topic><topic>Movement disorders</topic><topic>Necroptosis</topic><topic>Neostriatum</topic><topic>Neurobiology</topic><topic>Neurodegeneration</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neurosciences</topic><topic>Neurotoxicity</topic><topic>Oxidative stress</topic><topic>Oxygenase</topic><topic>Parkinson's disease</topic><topic>Peroxidation</topic><topic>Phenols</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Substantia Nigra - drug effects</topic><topic>Substantia Nigra - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Wei-Zhong</creatorcontrib><creatorcontrib>Wang, Hsiang-Tsui</creatorcontrib><creatorcontrib>Huang, Hui-Ju</creatorcontrib><creatorcontrib>Lo, Yu-Li</creatorcontrib><creatorcontrib>Lin, Anya Maan-Yuh</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Wei-Zhong</au><au>Wang, Hsiang-Tsui</au><au>Huang, Hui-Ju</au><au>Lo, Yu-Li</au><au>Lin, Anya Maan-Yuh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotective Effects of Baicalein on Acrolein-induced Neurotoxicity in the Nigrostriatal Dopaminergic System of Rat Brain</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2018</date><risdate>2018</risdate><volume>55</volume><issue>1</issue><spage>130</spage><epage>137</epage><pages>130-137</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Elevated levels of acrolein, an α,β-unsaturated aldehyde are detected in the brain of patients with Parkinson’s disease (PD). In the present study, the neuroprotective effect of baicalein (a phenolic flavonoid in the dried root of
Scutellaria baicalensis
Georgi) on acrolein-induced neurodegeneration of nigrostriatal dopaminergic system was investigated using local infusion of acrolein in the substantia nigra (SN) of rat brain. Systemic administration of baicalein (30 mg/kg, i.p.) significantly attenuated acrolein-induced elevations in 4-hydroxy-2-noneal (a product of lipid peroxidation), N-(3-formyl-3,4-dehydropiperidino)lysine (a biomarker of acrolein-conjugated proteins), and heme-oxygenase-1 levels (a redox-regulated protein) in the infused SN, indicating that baicalein inhibited acrolein-induced oxidative stress and protein conjugation. Furthermore, baicalein reduced acrolein-induced elevations in glial fibrillary acidic protein (a biomarker of activated astrocytes), ED-1 (a biomarker of activated microglia), and mature cathepsin B levels (a cysteine lysosomal protease), suggesting that baicalein attenuated acrolein-induced neuroinflammation. Moreover, baicalein attenuated acrolein-induced caspase 1 activation (a pro-inflammatory caspase) and interleukin-1β levels, indicating that baicalein prevented acrolein-induced inflammasome activation. In addition, baicalein significantly attenuated acrolein-induced caspase 3 activation (a biomarker of apoptosis) as well as acrolein-induced elevation in receptor interacting protein kinase (RIPK) 3 levels (an initiator of necroptosis), indicating that baicalein attenuated apoptosis and necroptosis. At the same time, baicalein mitigated acrolein-induced reduction in dopamine levels in the striatum ipsilateral to acrolein-infused SN. In conclusion, our data suggest that baicalein is neuroprotective via inhibiting oxidative stress, protein conjugation, and inflammation. Furthermore, baicalein prevents acrolein-induced program cell deaths, suggesting that baicalein is therapeutically useful for slowing PD progression.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>28866823</pmid><doi>10.1007/s12035-017-0725-x</doi><tpages>8</tpages></addata></record> |
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| subjects | Acrolein Acrolein - toxicity Animals Antioxidants - pharmacology Apoptosis Astrocytes Biomarkers Biomedical and Life Sciences Biomedicine Brain Caspase Caspase-1 Caspase-3 Cathepsin B Cell Biology Corpus Striatum - drug effects Corpus Striatum - metabolism Dopamine receptors Dopaminergic Neurons - drug effects Dopaminergic Neurons - metabolism Flavanones - pharmacology Glial fibrillary acidic protein Heme Inflammasomes Inflammation Kinases Lipid peroxidation Lysine Male Microglia Movement disorders Necroptosis Neostriatum Neurobiology Neurodegeneration Neurodegenerative diseases Neurology Neuroprotection Neuroprotective Agents - pharmacology Neurosciences Neurotoxicity Oxidative stress Oxygenase Parkinson's disease Peroxidation Phenols Protein kinase Proteins Rats Rats, Sprague-Dawley Rodents Substantia Nigra - drug effects Substantia Nigra - metabolism |
| title | Neuroprotective Effects of Baicalein on Acrolein-induced Neurotoxicity in the Nigrostriatal Dopaminergic System of Rat Brain |
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