Protopine ameliorates OVA-induced asthma through modulatingTLR4/MyD88/NF-κB pathway and NLRP3 inflammasome-mediated pyroptosis
Chronic airway inflammation and hyperresponsiveness are characteristics of asthma. The isoquinoline alkaloid protopine (PRO) has been shown to exert anti-inflammatory effects, but its mechanism of action in asthma is not known. Investigate the protective properties of PRO upon asthma and elucidate i...
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| Veröffentlicht in: | Phytomedicine (Stuttgart) 2024-04, Vol.126, p.155410-155410, Article 155410 |
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| creator | Yang, Jing Zhang, Meixian Luo, Yumeng Xu, Feng Gao, Fan Sun, Yanping Yang, Bingyou Kuang, Haixue |
| description | Chronic airway inflammation and hyperresponsiveness are characteristics of asthma. The isoquinoline alkaloid protopine (PRO) has been shown to exert anti-inflammatory effects, but its mechanism of action in asthma is not known.
Investigate the protective properties of PRO upon asthma and elucidate its mechanism.
The effects of PRO in asthma treatment were assessed by histology, biochemical analysis, and real-time reverse transcription-quantitative polymerase chain reaction. Then, we integrated molecular docking, western blotting, cellular experiments, immunohistochemistry, immunofluorescence analysis, flow cytometry, and metabolomics analysis to reveal its mechanism.
In vivo, PRO therapy reduced the number of inflammatory cells (eosinophils, leukocytes, monocytes) in bronchoalveolar lavage fluid (BALF), ameliorated pathologic alterations in lung tissues, and inhibited secretion of IgG and histamine. Molecular docking showed that PRO could dock with the proteins of TLR4, MyD88, TRAF6, TAK1, IKKα, and TNF-α. Western blotting displayed that PRO inhibited the TLR4/NF-κB signaling pathway. PRO regulated expression of the pyroptosis-related proteins NLR family pyrin domain containing 3 (NLRP3) inflammasome, gasdermin D, caspase-1, and drove caspase-1 inactivation to affect inflammatory responses by inhibiting the NLRP3 inflammasome. In vitro, 24 h after treatment with PRO, cell activity, as well as levels of reactive oxygen species (ROS) and interleukin (IL)-1β and IL-18, decreased significantly. Immunofluorescence staining showed that PRO decreased expression of TLR4 and MyD88 in vitro. PRO decreased nuclear translocation of NF-κB p65. Twenty-one potential biomarkers in serum were identified using metabolomics analysis, and they predominantly controlled the metabolism of phenylalanine, tryptophan, glucose, and sphingolipids.
PRO reduced OVA-induced asthma. The underlying mechanism was associated with the TLR4/MyD88/NF-κB pathway and NLRP3 inflammasome-mediated pyroptosis.
[Display omitted] |
| doi_str_mv | 10.1016/j.phymed.2024.155410 |
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Investigate the protective properties of PRO upon asthma and elucidate its mechanism.
The effects of PRO in asthma treatment were assessed by histology, biochemical analysis, and real-time reverse transcription-quantitative polymerase chain reaction. Then, we integrated molecular docking, western blotting, cellular experiments, immunohistochemistry, immunofluorescence analysis, flow cytometry, and metabolomics analysis to reveal its mechanism.
In vivo, PRO therapy reduced the number of inflammatory cells (eosinophils, leukocytes, monocytes) in bronchoalveolar lavage fluid (BALF), ameliorated pathologic alterations in lung tissues, and inhibited secretion of IgG and histamine. Molecular docking showed that PRO could dock with the proteins of TLR4, MyD88, TRAF6, TAK1, IKKα, and TNF-α. Western blotting displayed that PRO inhibited the TLR4/NF-κB signaling pathway. PRO regulated expression of the pyroptosis-related proteins NLR family pyrin domain containing 3 (NLRP3) inflammasome, gasdermin D, caspase-1, and drove caspase-1 inactivation to affect inflammatory responses by inhibiting the NLRP3 inflammasome. In vitro, 24 h after treatment with PRO, cell activity, as well as levels of reactive oxygen species (ROS) and interleukin (IL)-1β and IL-18, decreased significantly. Immunofluorescence staining showed that PRO decreased expression of TLR4 and MyD88 in vitro. PRO decreased nuclear translocation of NF-κB p65. Twenty-one potential biomarkers in serum were identified using metabolomics analysis, and they predominantly controlled the metabolism of phenylalanine, tryptophan, glucose, and sphingolipids.
PRO reduced OVA-induced asthma. The underlying mechanism was associated with the TLR4/MyD88/NF-κB pathway and NLRP3 inflammasome-mediated pyroptosis.
[Display omitted]</description><identifier>ISSN: 0944-7113</identifier><identifier>EISSN: 1618-095X</identifier><identifier>DOI: 10.1016/j.phymed.2024.155410</identifier><identifier>PMID: 38367422</identifier><language>eng</language><publisher>Germany: Elsevier GmbH</publisher><subject>alkaloids ; asthma ; Asthma - chemically induced ; Asthma - drug therapy ; Benzophenanthridines ; Berberine Alkaloids ; biomarkers ; blood serum ; Caspase 1 - metabolism ; caspase-1 ; domain ; eosinophils ; family ; flow cytometry ; fluorescent antibody technique ; glucose ; histamine ; Humans ; immunohistochemistry ; inflammasomes ; Inflammasomes - metabolism ; Inflammation ; interleukin-18 ; lungs ; mechanism of action ; metabolism ; Metabolomics ; Molecular docking ; Molecular Docking Simulation ; monocytes ; Myeloid Differentiation Factor 88 - metabolism ; NF-kappa B - metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; NLRP3 inflammasome ; Ovalbumin ; phenylalanine ; polymerase chain reaction ; Protopine ; Pyroptosis ; reactive oxygen species ; secretion ; sphingolipids ; therapeutics ; TLR4/NF-κB pathway ; Toll-Like Receptor 4 - metabolism ; tryptophan</subject><ispartof>Phytomedicine (Stuttgart), 2024-04, Vol.126, p.155410-155410, Article 155410</ispartof><rights>2024 The Author(s)</rights><rights>Copyright © 2024 The Author(s). Published by Elsevier GmbH.. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c390t-5a58b89bae5ed249801a009a40ca447c282c1132a1184cc76cb0673f948c70583</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0944711324000758$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38367422$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Jing</creatorcontrib><creatorcontrib>Zhang, Meixian</creatorcontrib><creatorcontrib>Luo, Yumeng</creatorcontrib><creatorcontrib>Xu, Feng</creatorcontrib><creatorcontrib>Gao, Fan</creatorcontrib><creatorcontrib>Sun, Yanping</creatorcontrib><creatorcontrib>Yang, Bingyou</creatorcontrib><creatorcontrib>Kuang, Haixue</creatorcontrib><title>Protopine ameliorates OVA-induced asthma through modulatingTLR4/MyD88/NF-κB pathway and NLRP3 inflammasome-mediated pyroptosis</title><title>Phytomedicine (Stuttgart)</title><addtitle>Phytomedicine</addtitle><description>Chronic airway inflammation and hyperresponsiveness are characteristics of asthma. The isoquinoline alkaloid protopine (PRO) has been shown to exert anti-inflammatory effects, but its mechanism of action in asthma is not known.
Investigate the protective properties of PRO upon asthma and elucidate its mechanism.
The effects of PRO in asthma treatment were assessed by histology, biochemical analysis, and real-time reverse transcription-quantitative polymerase chain reaction. Then, we integrated molecular docking, western blotting, cellular experiments, immunohistochemistry, immunofluorescence analysis, flow cytometry, and metabolomics analysis to reveal its mechanism.
In vivo, PRO therapy reduced the number of inflammatory cells (eosinophils, leukocytes, monocytes) in bronchoalveolar lavage fluid (BALF), ameliorated pathologic alterations in lung tissues, and inhibited secretion of IgG and histamine. Molecular docking showed that PRO could dock with the proteins of TLR4, MyD88, TRAF6, TAK1, IKKα, and TNF-α. Western blotting displayed that PRO inhibited the TLR4/NF-κB signaling pathway. PRO regulated expression of the pyroptosis-related proteins NLR family pyrin domain containing 3 (NLRP3) inflammasome, gasdermin D, caspase-1, and drove caspase-1 inactivation to affect inflammatory responses by inhibiting the NLRP3 inflammasome. In vitro, 24 h after treatment with PRO, cell activity, as well as levels of reactive oxygen species (ROS) and interleukin (IL)-1β and IL-18, decreased significantly. Immunofluorescence staining showed that PRO decreased expression of TLR4 and MyD88 in vitro. PRO decreased nuclear translocation of NF-κB p65. Twenty-one potential biomarkers in serum were identified using metabolomics analysis, and they predominantly controlled the metabolism of phenylalanine, tryptophan, glucose, and sphingolipids.
PRO reduced OVA-induced asthma. The underlying mechanism was associated with the TLR4/MyD88/NF-κB pathway and NLRP3 inflammasome-mediated pyroptosis.
[Display omitted]</description><subject>alkaloids</subject><subject>asthma</subject><subject>Asthma - chemically induced</subject><subject>Asthma - drug therapy</subject><subject>Benzophenanthridines</subject><subject>Berberine Alkaloids</subject><subject>biomarkers</subject><subject>blood serum</subject><subject>Caspase 1 - metabolism</subject><subject>caspase-1</subject><subject>domain</subject><subject>eosinophils</subject><subject>family</subject><subject>flow cytometry</subject><subject>fluorescent antibody technique</subject><subject>glucose</subject><subject>histamine</subject><subject>Humans</subject><subject>immunohistochemistry</subject><subject>inflammasomes</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammation</subject><subject>interleukin-18</subject><subject>lungs</subject><subject>mechanism of action</subject><subject>metabolism</subject><subject>Metabolomics</subject><subject>Molecular docking</subject><subject>Molecular Docking Simulation</subject><subject>monocytes</subject><subject>Myeloid Differentiation Factor 88 - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>NLRP3 inflammasome</subject><subject>Ovalbumin</subject><subject>phenylalanine</subject><subject>polymerase chain reaction</subject><subject>Protopine</subject><subject>Pyroptosis</subject><subject>reactive oxygen species</subject><subject>secretion</subject><subject>sphingolipids</subject><subject>therapeutics</subject><subject>TLR4/NF-κB pathway</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>tryptophan</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>eNqFkc9u1DAQhy0EokvhDRDykUt2_S-JfUEqhQLS0lZVQdysWcfbeJXEwXZAOfFePATPhFdpr3Cag7-Z34w_hF5SsqaEVpvDemzn3jZrRphY07IUlDxCK1pRWRBVfnuMVkQJUdSU8hP0LMYDIVSomjxFJ1zyqhaMrdCv6-CTH91gMfS2cz5AshFffT0r3NBMxjYYYmp7wKkNfrprce-bqYPkhrvb7Y3YfJ7fSbm5vCj-_H6LR0jtT5gxDA2-3N5cc-yGfQd9D9H3tsjbujy-weMc_Jh8dPE5erKHLtoX9_UUfbl4f3v-sdheffh0frYtDFckFSWUcifVDmxpGyaUJBQIUSCIASFqwyQz-U4GlEphTF2ZHalqvldCmpqUkp-i18vcMfjvk41J9y4a23UwWD9FzWnJK8q5qP-LMpXTxJHMqFhQE3yMwe71GFwPYdaU6KMlfdCLJX20pBdLue3VfcK0O749ND1oycCbBbD5S344G3Q0zg7ZhgvWJN149--EvxLapXQ</recordid><startdate>202404</startdate><enddate>202404</enddate><creator>Yang, Jing</creator><creator>Zhang, Meixian</creator><creator>Luo, Yumeng</creator><creator>Xu, Feng</creator><creator>Gao, Fan</creator><creator>Sun, Yanping</creator><creator>Yang, Bingyou</creator><creator>Kuang, Haixue</creator><general>Elsevier GmbH</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></search><sort><creationdate>202404</creationdate><title>Protopine ameliorates OVA-induced asthma through modulatingTLR4/MyD88/NF-κB pathway and NLRP3 inflammasome-mediated pyroptosis</title><author>Yang, Jing ; Zhang, Meixian ; Luo, Yumeng ; Xu, Feng ; Gao, Fan ; Sun, Yanping ; Yang, Bingyou ; Kuang, Haixue</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-5a58b89bae5ed249801a009a40ca447c282c1132a1184cc76cb0673f948c70583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>alkaloids</topic><topic>asthma</topic><topic>Asthma - chemically induced</topic><topic>Asthma - drug therapy</topic><topic>Benzophenanthridines</topic><topic>Berberine Alkaloids</topic><topic>biomarkers</topic><topic>blood serum</topic><topic>Caspase 1 - metabolism</topic><topic>caspase-1</topic><topic>domain</topic><topic>eosinophils</topic><topic>family</topic><topic>flow cytometry</topic><topic>fluorescent antibody technique</topic><topic>glucose</topic><topic>histamine</topic><topic>Humans</topic><topic>immunohistochemistry</topic><topic>inflammasomes</topic><topic>Inflammasomes - metabolism</topic><topic>Inflammation</topic><topic>interleukin-18</topic><topic>lungs</topic><topic>mechanism of action</topic><topic>metabolism</topic><topic>Metabolomics</topic><topic>Molecular docking</topic><topic>Molecular Docking Simulation</topic><topic>monocytes</topic><topic>Myeloid Differentiation Factor 88 - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>NLRP3 inflammasome</topic><topic>Ovalbumin</topic><topic>phenylalanine</topic><topic>polymerase chain reaction</topic><topic>Protopine</topic><topic>Pyroptosis</topic><topic>reactive oxygen species</topic><topic>secretion</topic><topic>sphingolipids</topic><topic>therapeutics</topic><topic>TLR4/NF-κB pathway</topic><topic>Toll-Like Receptor 4 - metabolism</topic><topic>tryptophan</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Jing</creatorcontrib><creatorcontrib>Zhang, Meixian</creatorcontrib><creatorcontrib>Luo, Yumeng</creatorcontrib><creatorcontrib>Xu, Feng</creatorcontrib><creatorcontrib>Gao, Fan</creatorcontrib><creatorcontrib>Sun, Yanping</creatorcontrib><creatorcontrib>Yang, Bingyou</creatorcontrib><creatorcontrib>Kuang, Haixue</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>Phytomedicine (Stuttgart)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Jing</au><au>Zhang, Meixian</au><au>Luo, Yumeng</au><au>Xu, Feng</au><au>Gao, Fan</au><au>Sun, Yanping</au><au>Yang, Bingyou</au><au>Kuang, Haixue</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protopine ameliorates OVA-induced asthma through modulatingTLR4/MyD88/NF-κB pathway and NLRP3 inflammasome-mediated pyroptosis</atitle><jtitle>Phytomedicine (Stuttgart)</jtitle><addtitle>Phytomedicine</addtitle><date>2024-04</date><risdate>2024</risdate><volume>126</volume><spage>155410</spage><epage>155410</epage><pages>155410-155410</pages><artnum>155410</artnum><issn>0944-7113</issn><eissn>1618-095X</eissn><abstract>Chronic airway inflammation and hyperresponsiveness are characteristics of asthma. The isoquinoline alkaloid protopine (PRO) has been shown to exert anti-inflammatory effects, but its mechanism of action in asthma is not known.
Investigate the protective properties of PRO upon asthma and elucidate its mechanism.
The effects of PRO in asthma treatment were assessed by histology, biochemical analysis, and real-time reverse transcription-quantitative polymerase chain reaction. Then, we integrated molecular docking, western blotting, cellular experiments, immunohistochemistry, immunofluorescence analysis, flow cytometry, and metabolomics analysis to reveal its mechanism.
In vivo, PRO therapy reduced the number of inflammatory cells (eosinophils, leukocytes, monocytes) in bronchoalveolar lavage fluid (BALF), ameliorated pathologic alterations in lung tissues, and inhibited secretion of IgG and histamine. Molecular docking showed that PRO could dock with the proteins of TLR4, MyD88, TRAF6, TAK1, IKKα, and TNF-α. Western blotting displayed that PRO inhibited the TLR4/NF-κB signaling pathway. PRO regulated expression of the pyroptosis-related proteins NLR family pyrin domain containing 3 (NLRP3) inflammasome, gasdermin D, caspase-1, and drove caspase-1 inactivation to affect inflammatory responses by inhibiting the NLRP3 inflammasome. In vitro, 24 h after treatment with PRO, cell activity, as well as levels of reactive oxygen species (ROS) and interleukin (IL)-1β and IL-18, decreased significantly. Immunofluorescence staining showed that PRO decreased expression of TLR4 and MyD88 in vitro. PRO decreased nuclear translocation of NF-κB p65. Twenty-one potential biomarkers in serum were identified using metabolomics analysis, and they predominantly controlled the metabolism of phenylalanine, tryptophan, glucose, and sphingolipids.
PRO reduced OVA-induced asthma. The underlying mechanism was associated with the TLR4/MyD88/NF-κB pathway and NLRP3 inflammasome-mediated pyroptosis.
[Display omitted]</abstract><cop>Germany</cop><pub>Elsevier GmbH</pub><pmid>38367422</pmid><doi>10.1016/j.phymed.2024.155410</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | alkaloids asthma Asthma - chemically induced Asthma - drug therapy Benzophenanthridines Berberine Alkaloids biomarkers blood serum Caspase 1 - metabolism caspase-1 domain eosinophils family flow cytometry fluorescent antibody technique glucose histamine Humans immunohistochemistry inflammasomes Inflammasomes - metabolism Inflammation interleukin-18 lungs mechanism of action metabolism Metabolomics Molecular docking Molecular Docking Simulation monocytes Myeloid Differentiation Factor 88 - metabolism NF-kappa B - metabolism NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 inflammasome Ovalbumin phenylalanine polymerase chain reaction Protopine Pyroptosis reactive oxygen species secretion sphingolipids therapeutics TLR4/NF-κB pathway Toll-Like Receptor 4 - metabolism tryptophan |
| title | Protopine ameliorates OVA-induced asthma through modulatingTLR4/MyD88/NF-κB pathway and NLRP3 inflammasome-mediated pyroptosis |
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