Baohuoside I suppresses the NLRP3 inflammasome activation via targeting GPER to fight against Parkinson's disease
Accumulating evidence indicates the crucial role of microglia-mediated inflammation and the NLR family pyrin domain containing 3 (NLRP3) inflammasome-mediated pyroptosis in the pathogenesis of Parkinson's disease (PD). Baohuoside I, a natural flavonoid extracted from Herba Epimedii, has been sh...
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| description | Accumulating evidence indicates the crucial role of microglia-mediated inflammation and the NLR family pyrin domain containing 3 (NLRP3) inflammasome-mediated pyroptosis in the pathogenesis of Parkinson's disease (PD). Baohuoside I, a natural flavonoid extracted from Herba Epimedii, has been shown to possess anti-inflammatory effects, but its potential neuroprotective effects and mechanism against PD have not been documented.
The anti-inflammatory effects of Baohuoside I were evaluated by LPS-induced BV2 cells or primary microglia isolated from wide type or G protein-coupled estrogen receptor (GPER) gene knockout mice. The underlying mechanism related to GPER-mediated NLRP3 inflammasome inhibition was further explored using LPS-induced GPER+/+ or GPER−/− mouse models of PD. The neuroprotective effects of Baohuoside I were detected through western blot analysis, real-time PCR, molecular docking, mouse behavioral tests, immunofluorescence, and immunohistochemistry.
Baohuoside I significantly alleviated LPS-induced neuroinflammation by inhibiting the activation of NF-κB signal and the increase of pyroptosis levels as evidenced by the downregulated expression of pyroptosis-related proteins (NLRP3, ASC, pro-Caspase-1, IL-1β) in microglia cells. Intragastric administration of Baohuoside I protected against LPS-induced motor dysfunction and loss of dopaminergic neurons, reduced pro-inflammatory cytokines expressions, and inhibited microglial (Iba-1) and astrocyte (GFAP) activation in the nigrostriatal pathway in LPS-induced mouse model of PD. Pretreatment with GPER antagonist G15 in microglia cells or GPER gene deletion in mice significantly blocked the inhibitory effects of Baohuoside I on LPS-induced neuroinflammation and activation of the NLRP3/ASC/Caspase-1 pathway. Molecular docking further indicated that Baohuoside I might bind to GPER directly with a binding energy of -10.4 kcal/mol.
Baohuoside I provides neuroprotective effects against PD by inhibiting the activation of the NF-κB signal and NLRP3/ASC/Caspase-1 pathway. The molecular target for its anti-inflammatory effects is proved to be GPER in the PD mouse model. Baohuoside I may be a valuable anti-neuroinflammatory agent and a drug with well-defined target for the treatment of PD.
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| doi_str_mv | 10.1016/j.phymed.2024.155435 |
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The anti-inflammatory effects of Baohuoside I were evaluated by LPS-induced BV2 cells or primary microglia isolated from wide type or G protein-coupled estrogen receptor (GPER) gene knockout mice. The underlying mechanism related to GPER-mediated NLRP3 inflammasome inhibition was further explored using LPS-induced GPER+/+ or GPER−/− mouse models of PD. The neuroprotective effects of Baohuoside I were detected through western blot analysis, real-time PCR, molecular docking, mouse behavioral tests, immunofluorescence, and immunohistochemistry.
Baohuoside I significantly alleviated LPS-induced neuroinflammation by inhibiting the activation of NF-κB signal and the increase of pyroptosis levels as evidenced by the downregulated expression of pyroptosis-related proteins (NLRP3, ASC, pro-Caspase-1, IL-1β) in microglia cells. Intragastric administration of Baohuoside I protected against LPS-induced motor dysfunction and loss of dopaminergic neurons, reduced pro-inflammatory cytokines expressions, and inhibited microglial (Iba-1) and astrocyte (GFAP) activation in the nigrostriatal pathway in LPS-induced mouse model of PD. Pretreatment with GPER antagonist G15 in microglia cells or GPER gene deletion in mice significantly blocked the inhibitory effects of Baohuoside I on LPS-induced neuroinflammation and activation of the NLRP3/ASC/Caspase-1 pathway. Molecular docking further indicated that Baohuoside I might bind to GPER directly with a binding energy of -10.4 kcal/mol.
Baohuoside I provides neuroprotective effects against PD by inhibiting the activation of the NF-κB signal and NLRP3/ASC/Caspase-1 pathway. The molecular target for its anti-inflammatory effects is proved to be GPER in the PD mouse model. Baohuoside I may be a valuable anti-neuroinflammatory agent and a drug with well-defined target for the treatment of PD.
[Display omitted]</description><identifier>ISSN: 0944-7113</identifier><identifier>EISSN: 1618-095X</identifier><identifier>DOI: 10.1016/j.phymed.2024.155435</identifier><identifier>PMID: 38394727</identifier><language>eng</language><publisher>Germany: Elsevier GmbH</publisher><subject>Animals ; antagonists ; Anti-Inflammatory Agents - metabolism ; Anti-Inflammatory Agents - pharmacology ; astrocytes ; Baohuoside I ; Caspases - metabolism ; cytokines ; domain ; drugs ; energy ; estrogen receptors ; family ; flavonoids ; Flavonoids - pharmacology ; fluorescent antibody technique ; G protein-coupled estrogen receptor ; gene deletion ; gene targeting ; Icariside II ; immunohistochemistry ; Inflammasomes ; inflammation ; intragastric administration ; Lipopolysaccharides - pharmacology ; Mice ; Mice, Inbred C57BL ; Microglia ; Molecular Docking Simulation ; Neuroinflammatory Diseases ; Neuroprotective Agents - pharmacology ; NF-kappa B - metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; NLRP3 inflammasome ; Parkinson disease ; Parkinson Disease - drug therapy ; Parkinson Disease - metabolism ; Parkinson's disease ; pathogenesis ; pyroptosis ; quantitative polymerase chain reaction ; Receptors, G-Protein-Coupled - metabolism ; Western blotting</subject><ispartof>Phytomedicine (Stuttgart), 2024-04, Vol.126, p.155435-155435, Article 155435</ispartof><rights>2024 Elsevier GmbH</rights><rights>Copyright © 2024 Elsevier GmbH. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c344t-c01e231cb0347e5aa6d1fc17b018daaef746e991566281906b32cd726f7778f33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0944711324001004$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38394727$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gu, Yu</creatorcontrib><creatorcontrib>Hu, Zi-Fan</creatorcontrib><creatorcontrib>Zheng, Dan-Wen</creatorcontrib><creatorcontrib>Yang, Yan-Qing</creatorcontrib><creatorcontrib>Dong, Xiao-Li</creatorcontrib><creatorcontrib>Chen, Wen-Fang</creatorcontrib><title>Baohuoside I suppresses the NLRP3 inflammasome activation via targeting GPER to fight against Parkinson's disease</title><title>Phytomedicine (Stuttgart)</title><addtitle>Phytomedicine</addtitle><description>Accumulating evidence indicates the crucial role of microglia-mediated inflammation and the NLR family pyrin domain containing 3 (NLRP3) inflammasome-mediated pyroptosis in the pathogenesis of Parkinson's disease (PD). Baohuoside I, a natural flavonoid extracted from Herba Epimedii, has been shown to possess anti-inflammatory effects, but its potential neuroprotective effects and mechanism against PD have not been documented.
The anti-inflammatory effects of Baohuoside I were evaluated by LPS-induced BV2 cells or primary microglia isolated from wide type or G protein-coupled estrogen receptor (GPER) gene knockout mice. The underlying mechanism related to GPER-mediated NLRP3 inflammasome inhibition was further explored using LPS-induced GPER+/+ or GPER−/− mouse models of PD. The neuroprotective effects of Baohuoside I were detected through western blot analysis, real-time PCR, molecular docking, mouse behavioral tests, immunofluorescence, and immunohistochemistry.
Baohuoside I significantly alleviated LPS-induced neuroinflammation by inhibiting the activation of NF-κB signal and the increase of pyroptosis levels as evidenced by the downregulated expression of pyroptosis-related proteins (NLRP3, ASC, pro-Caspase-1, IL-1β) in microglia cells. Intragastric administration of Baohuoside I protected against LPS-induced motor dysfunction and loss of dopaminergic neurons, reduced pro-inflammatory cytokines expressions, and inhibited microglial (Iba-1) and astrocyte (GFAP) activation in the nigrostriatal pathway in LPS-induced mouse model of PD. Pretreatment with GPER antagonist G15 in microglia cells or GPER gene deletion in mice significantly blocked the inhibitory effects of Baohuoside I on LPS-induced neuroinflammation and activation of the NLRP3/ASC/Caspase-1 pathway. Molecular docking further indicated that Baohuoside I might bind to GPER directly with a binding energy of -10.4 kcal/mol.
Baohuoside I provides neuroprotective effects against PD by inhibiting the activation of the NF-κB signal and NLRP3/ASC/Caspase-1 pathway. The molecular target for its anti-inflammatory effects is proved to be GPER in the PD mouse model. Baohuoside I may be a valuable anti-neuroinflammatory agent and a drug with well-defined target for the treatment of PD.
[Display omitted]</description><subject>Animals</subject><subject>antagonists</subject><subject>Anti-Inflammatory Agents - metabolism</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>astrocytes</subject><subject>Baohuoside I</subject><subject>Caspases - metabolism</subject><subject>cytokines</subject><subject>domain</subject><subject>drugs</subject><subject>energy</subject><subject>estrogen receptors</subject><subject>family</subject><subject>flavonoids</subject><subject>Flavonoids - pharmacology</subject><subject>fluorescent antibody technique</subject><subject>G protein-coupled estrogen receptor</subject><subject>gene deletion</subject><subject>gene targeting</subject><subject>Icariside II</subject><subject>immunohistochemistry</subject><subject>Inflammasomes</subject><subject>inflammation</subject><subject>intragastric administration</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microglia</subject><subject>Molecular Docking Simulation</subject><subject>Neuroinflammatory Diseases</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>NF-kappa B - metabolism</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>NLRP3 inflammasome</subject><subject>Parkinson disease</subject><subject>Parkinson Disease - drug therapy</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinson's disease</subject><subject>pathogenesis</subject><subject>pyroptosis</subject><subject>quantitative polymerase chain reaction</subject><subject>Receptors, G-Protein-Coupled - metabolism</subject><subject>Western blotting</subject><issn>0944-7113</issn><issn>1618-095X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcGO0zAQhi0EYsvCGyDkG1xSPLEdJxckWC3LShVUK5C4Wa4zaV2aOOtxKu3bk6q7VzjNSPP9M9J8jL0FsQQB1cf9ctw99NguS1GqJWitpH7GFlBBXYhG_37OFqJRqjAA8oK9ItoLAaox4iW7kLVslCnNgt1_cXE3RQot8ltO0zgmJELieYf8--puLXkYuoPre0exR-58DkeXQxz4MTieXdpiDsOW36yv73iOvAvbXeZu68JAma9d-jM3cXhPvA2EjvA1e9G5A-Gbx3rJfn29_nn1rVj9uLm9-rwqvFQqF14AlhL8RkhlUDtXtdB5MBsBdescdkZV2DSgq6qsoRHVRpa-NWXVGWPqTspL9uG8d0zxfkLKtg_k8XBwA8aJrAQtdWMqMP9Fy0areavWJ1SdUZ8iUcLOjin0Lj1YEPbkxe7t2Ys9ebFnL3Ps3eOFaXOaPYWeRMzApzOA80uOAZMlH3Dw2IaEPts2hn9f-AuUwaBe</recordid><startdate>202404</startdate><enddate>202404</enddate><creator>Gu, Yu</creator><creator>Hu, Zi-Fan</creator><creator>Zheng, Dan-Wen</creator><creator>Yang, Yan-Qing</creator><creator>Dong, Xiao-Li</creator><creator>Chen, Wen-Fang</creator><general>Elsevier GmbH</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><scope>7S9</scope><scope>L.6</scope></search><sort><creationdate>202404</creationdate><title>Baohuoside I suppresses the NLRP3 inflammasome activation via targeting GPER to fight against Parkinson's disease</title><author>Gu, Yu ; Hu, Zi-Fan ; Zheng, Dan-Wen ; Yang, Yan-Qing ; Dong, Xiao-Li ; Chen, Wen-Fang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c344t-c01e231cb0347e5aa6d1fc17b018daaef746e991566281906b32cd726f7778f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>antagonists</topic><topic>Anti-Inflammatory Agents - metabolism</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>astrocytes</topic><topic>Baohuoside I</topic><topic>Caspases - metabolism</topic><topic>cytokines</topic><topic>domain</topic><topic>drugs</topic><topic>energy</topic><topic>estrogen receptors</topic><topic>family</topic><topic>flavonoids</topic><topic>Flavonoids - pharmacology</topic><topic>fluorescent antibody technique</topic><topic>G protein-coupled estrogen receptor</topic><topic>gene deletion</topic><topic>gene targeting</topic><topic>Icariside II</topic><topic>immunohistochemistry</topic><topic>Inflammasomes</topic><topic>inflammation</topic><topic>intragastric administration</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microglia</topic><topic>Molecular Docking Simulation</topic><topic>Neuroinflammatory Diseases</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>NF-kappa B - metabolism</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>NLRP3 inflammasome</topic><topic>Parkinson disease</topic><topic>Parkinson Disease - drug therapy</topic><topic>Parkinson Disease - metabolism</topic><topic>Parkinson's disease</topic><topic>pathogenesis</topic><topic>pyroptosis</topic><topic>quantitative polymerase chain reaction</topic><topic>Receptors, G-Protein-Coupled - metabolism</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gu, Yu</creatorcontrib><creatorcontrib>Hu, Zi-Fan</creatorcontrib><creatorcontrib>Zheng, Dan-Wen</creatorcontrib><creatorcontrib>Yang, Yan-Qing</creatorcontrib><creatorcontrib>Dong, Xiao-Li</creatorcontrib><creatorcontrib>Chen, Wen-Fang</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><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Phytomedicine (Stuttgart)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gu, Yu</au><au>Hu, Zi-Fan</au><au>Zheng, Dan-Wen</au><au>Yang, Yan-Qing</au><au>Dong, Xiao-Li</au><au>Chen, Wen-Fang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Baohuoside I suppresses the NLRP3 inflammasome activation via targeting GPER to fight against Parkinson's disease</atitle><jtitle>Phytomedicine (Stuttgart)</jtitle><addtitle>Phytomedicine</addtitle><date>2024-04</date><risdate>2024</risdate><volume>126</volume><spage>155435</spage><epage>155435</epage><pages>155435-155435</pages><artnum>155435</artnum><issn>0944-7113</issn><eissn>1618-095X</eissn><abstract>Accumulating evidence indicates the crucial role of microglia-mediated inflammation and the NLR family pyrin domain containing 3 (NLRP3) inflammasome-mediated pyroptosis in the pathogenesis of Parkinson's disease (PD). Baohuoside I, a natural flavonoid extracted from Herba Epimedii, has been shown to possess anti-inflammatory effects, but its potential neuroprotective effects and mechanism against PD have not been documented.
The anti-inflammatory effects of Baohuoside I were evaluated by LPS-induced BV2 cells or primary microglia isolated from wide type or G protein-coupled estrogen receptor (GPER) gene knockout mice. The underlying mechanism related to GPER-mediated NLRP3 inflammasome inhibition was further explored using LPS-induced GPER+/+ or GPER−/− mouse models of PD. The neuroprotective effects of Baohuoside I were detected through western blot analysis, real-time PCR, molecular docking, mouse behavioral tests, immunofluorescence, and immunohistochemistry.
Baohuoside I significantly alleviated LPS-induced neuroinflammation by inhibiting the activation of NF-κB signal and the increase of pyroptosis levels as evidenced by the downregulated expression of pyroptosis-related proteins (NLRP3, ASC, pro-Caspase-1, IL-1β) in microglia cells. Intragastric administration of Baohuoside I protected against LPS-induced motor dysfunction and loss of dopaminergic neurons, reduced pro-inflammatory cytokines expressions, and inhibited microglial (Iba-1) and astrocyte (GFAP) activation in the nigrostriatal pathway in LPS-induced mouse model of PD. Pretreatment with GPER antagonist G15 in microglia cells or GPER gene deletion in mice significantly blocked the inhibitory effects of Baohuoside I on LPS-induced neuroinflammation and activation of the NLRP3/ASC/Caspase-1 pathway. Molecular docking further indicated that Baohuoside I might bind to GPER directly with a binding energy of -10.4 kcal/mol.
Baohuoside I provides neuroprotective effects against PD by inhibiting the activation of the NF-κB signal and NLRP3/ASC/Caspase-1 pathway. The molecular target for its anti-inflammatory effects is proved to be GPER in the PD mouse model. Baohuoside I may be a valuable anti-neuroinflammatory agent and a drug with well-defined target for the treatment of PD.
[Display omitted]</abstract><cop>Germany</cop><pub>Elsevier GmbH</pub><pmid>38394727</pmid><doi>10.1016/j.phymed.2024.155435</doi><tpages>1</tpages></addata></record> |
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| subjects | Animals antagonists Anti-Inflammatory Agents - metabolism Anti-Inflammatory Agents - pharmacology astrocytes Baohuoside I Caspases - metabolism cytokines domain drugs energy estrogen receptors family flavonoids Flavonoids - pharmacology fluorescent antibody technique G protein-coupled estrogen receptor gene deletion gene targeting Icariside II immunohistochemistry Inflammasomes inflammation intragastric administration Lipopolysaccharides - pharmacology Mice Mice, Inbred C57BL Microglia Molecular Docking Simulation Neuroinflammatory Diseases Neuroprotective Agents - pharmacology NF-kappa B - metabolism NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 inflammasome Parkinson disease Parkinson Disease - drug therapy Parkinson Disease - metabolism Parkinson's disease pathogenesis pyroptosis quantitative polymerase chain reaction Receptors, G-Protein-Coupled - metabolism Western blotting |
| title | Baohuoside I suppresses the NLRP3 inflammasome activation via targeting GPER to fight against Parkinson's disease |
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