Paeonol Alleviates Subarachnoid Hemorrhage Injury in Rats Through Upregulation of SIRT1 and Inhibition of HMGB1/TLR4/MyD88/NF‐κB Pathway
ABSTRACT Paeonol is a principle bioactive compound separated from the root bark of Cortex Moutan and has been shown to confer various biological functions, including antineuroinflammation and neuroprotection. Inflammation, blood–brain barrier (BBB), permeability, and apoptosis are three major underl...
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| creator | Liu, Zhao Zhu, Jun Pan, Enyu Pang, Lujun Zhou, Xiwei Che, Yanjun |
| description | ABSTRACT
Paeonol is a principle bioactive compound separated from the root bark of Cortex Moutan and has been shown to confer various biological functions, including antineuroinflammation and neuroprotection. Inflammation, blood–brain barrier (BBB), permeability, and apoptosis are three major underlying mechanisms involved in early brain injury (EBI) postsubarachnoid hemorrhage (SAH). This study aimed to detect the roles and mechanisms of paeonol in EBI following SAH. A SAH model was established by an endovascular perforation method in Sprague‐Dawley rats. The localizations of HMGB1 and p65 were identified by immunofluorescence staining. Protein levels were measured by western blot analysis. The serum levels of HMGB1 and the levels of inflammatory cytokines in the brain cortex were evaluated by ELISA. Hematoxylin and eosin staining was conducted to detect neuronal degeneration. Brain water content and Evans blue extravasation were assessed to determine EBI. Neuronal apoptosis was examined by TUNEL. Paeonol deacetylated HMGB1 by upregulating SIRT1 level. SIRT1 inhibition attenuated the protective effects of paeonol against neurological dysfunctions, brain edema, and BBB disruption. SIRT1 inhibition rescued the paeonol‐induced inhibition in inflammatory response. The paeonol‐induced decrease in neuronal apoptosis was restored by SIRT1 inhibitor. The paeonol‐mediated deactivated TLR4/MyD88/NF‐κB pathway was activated by SIRT1 inhibitor. Paeonol alleviates the SAH injury in rats by upregulating SIRT1 to inactivate the HMGB1/TLR4/MyD88/NF‐κB pathway.
Scientific diagram demonstrating the underlying mechanisms involving in neuroprotective effects of paeonol. |
| doi_str_mv | 10.1002/jbt.70035 |
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Paeonol is a principle bioactive compound separated from the root bark of Cortex Moutan and has been shown to confer various biological functions, including antineuroinflammation and neuroprotection. Inflammation, blood–brain barrier (BBB), permeability, and apoptosis are three major underlying mechanisms involved in early brain injury (EBI) postsubarachnoid hemorrhage (SAH). This study aimed to detect the roles and mechanisms of paeonol in EBI following SAH. A SAH model was established by an endovascular perforation method in Sprague‐Dawley rats. The localizations of HMGB1 and p65 were identified by immunofluorescence staining. Protein levels were measured by western blot analysis. The serum levels of HMGB1 and the levels of inflammatory cytokines in the brain cortex were evaluated by ELISA. Hematoxylin and eosin staining was conducted to detect neuronal degeneration. Brain water content and Evans blue extravasation were assessed to determine EBI. Neuronal apoptosis was examined by TUNEL. Paeonol deacetylated HMGB1 by upregulating SIRT1 level. SIRT1 inhibition attenuated the protective effects of paeonol against neurological dysfunctions, brain edema, and BBB disruption. SIRT1 inhibition rescued the paeonol‐induced inhibition in inflammatory response. The paeonol‐induced decrease in neuronal apoptosis was restored by SIRT1 inhibitor. The paeonol‐mediated deactivated TLR4/MyD88/NF‐κB pathway was activated by SIRT1 inhibitor. Paeonol alleviates the SAH injury in rats by upregulating SIRT1 to inactivate the HMGB1/TLR4/MyD88/NF‐κB pathway.
Scientific diagram demonstrating the underlying mechanisms involving in neuroprotective effects of paeonol.</description><identifier>ISSN: 1095-6670</identifier><identifier>ISSN: 1099-0461</identifier><identifier>EISSN: 1099-0461</identifier><identifier>DOI: 10.1002/jbt.70035</identifier><identifier>PMID: 39552449</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Acetophenones - pharmacology ; Animals ; Apoptosis ; Apoptosis - drug effects ; Bioactive compounds ; Blood-brain barrier ; Blood-Brain Barrier - drug effects ; Blood-Brain Barrier - metabolism ; Brain injury ; Cardiovascular system ; Degeneration ; Edema ; Enzyme-linked immunosorbent assay ; Extravasation ; Head injuries ; Hemorrhage ; HMGB1 ; HMGB1 protein ; HMGB1 Protein - metabolism ; Immunofluorescence ; Inflammation ; Inflammatory response ; Inhibitors ; Injury analysis ; Male ; Membrane permeability ; Moisture content ; MyD88 protein ; Myeloid Differentiation Factor 88 - metabolism ; Neurodegeneration ; Neurological diseases ; Neuroprotection ; NF-kappa B - metabolism ; NF‐κB ; paeonol ; Rats ; Rats, Sprague-Dawley ; Serum levels ; Signal Transduction - drug effects ; SIRT1 ; SIRT1 protein ; Sirtuin 1 - metabolism ; Staining ; Stroke ; Subarachnoid hemorrhage ; Subarachnoid Hemorrhage - drug therapy ; Subarachnoid Hemorrhage - metabolism ; Subarachnoid Hemorrhage - pathology ; TLR4 protein ; Toll-Like Receptor 4 - metabolism ; Toll-like receptors ; Up-Regulation - drug effects ; Water content</subject><ispartof>Journal of biochemical and molecular toxicology, 2024-12, Vol.38 (12), p.e70035-n/a</ispartof><rights>2024 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c2435-efa193d3eb772143128dc98d5d0042807ac0329788026dfb5f33fe56eaec6e783</cites><orcidid>0009-0003-3551-8424</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%2Fjbt.70035$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjbt.70035$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39552449$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Zhao</creatorcontrib><creatorcontrib>Zhu, Jun</creatorcontrib><creatorcontrib>Pan, Enyu</creatorcontrib><creatorcontrib>Pang, Lujun</creatorcontrib><creatorcontrib>Zhou, Xiwei</creatorcontrib><creatorcontrib>Che, Yanjun</creatorcontrib><title>Paeonol Alleviates Subarachnoid Hemorrhage Injury in Rats Through Upregulation of SIRT1 and Inhibition of HMGB1/TLR4/MyD88/NF‐κB Pathway</title><title>Journal of biochemical and molecular toxicology</title><addtitle>J Biochem Mol Toxicol</addtitle><description>ABSTRACT
Paeonol is a principle bioactive compound separated from the root bark of Cortex Moutan and has been shown to confer various biological functions, including antineuroinflammation and neuroprotection. Inflammation, blood–brain barrier (BBB), permeability, and apoptosis are three major underlying mechanisms involved in early brain injury (EBI) postsubarachnoid hemorrhage (SAH). This study aimed to detect the roles and mechanisms of paeonol in EBI following SAH. A SAH model was established by an endovascular perforation method in Sprague‐Dawley rats. The localizations of HMGB1 and p65 were identified by immunofluorescence staining. Protein levels were measured by western blot analysis. The serum levels of HMGB1 and the levels of inflammatory cytokines in the brain cortex were evaluated by ELISA. Hematoxylin and eosin staining was conducted to detect neuronal degeneration. Brain water content and Evans blue extravasation were assessed to determine EBI. Neuronal apoptosis was examined by TUNEL. Paeonol deacetylated HMGB1 by upregulating SIRT1 level. SIRT1 inhibition attenuated the protective effects of paeonol against neurological dysfunctions, brain edema, and BBB disruption. SIRT1 inhibition rescued the paeonol‐induced inhibition in inflammatory response. The paeonol‐induced decrease in neuronal apoptosis was restored by SIRT1 inhibitor. The paeonol‐mediated deactivated TLR4/MyD88/NF‐κB pathway was activated by SIRT1 inhibitor. Paeonol alleviates the SAH injury in rats by upregulating SIRT1 to inactivate the HMGB1/TLR4/MyD88/NF‐κB pathway.
Scientific diagram demonstrating the underlying mechanisms involving in neuroprotective effects of paeonol.</description><subject>Acetophenones - pharmacology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Bioactive compounds</subject><subject>Blood-brain barrier</subject><subject>Blood-Brain Barrier - drug effects</subject><subject>Blood-Brain Barrier - metabolism</subject><subject>Brain injury</subject><subject>Cardiovascular system</subject><subject>Degeneration</subject><subject>Edema</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Extravasation</subject><subject>Head injuries</subject><subject>Hemorrhage</subject><subject>HMGB1</subject><subject>HMGB1 protein</subject><subject>HMGB1 Protein - metabolism</subject><subject>Immunofluorescence</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Inhibitors</subject><subject>Injury analysis</subject><subject>Male</subject><subject>Membrane permeability</subject><subject>Moisture content</subject><subject>MyD88 protein</subject><subject>Myeloid Differentiation Factor 88 - metabolism</subject><subject>Neurodegeneration</subject><subject>Neurological diseases</subject><subject>Neuroprotection</subject><subject>NF-kappa B - metabolism</subject><subject>NF‐κB</subject><subject>paeonol</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Serum levels</subject><subject>Signal Transduction - drug effects</subject><subject>SIRT1</subject><subject>SIRT1 protein</subject><subject>Sirtuin 1 - metabolism</subject><subject>Staining</subject><subject>Stroke</subject><subject>Subarachnoid hemorrhage</subject><subject>Subarachnoid Hemorrhage - drug therapy</subject><subject>Subarachnoid Hemorrhage - metabolism</subject><subject>Subarachnoid Hemorrhage - pathology</subject><subject>TLR4 protein</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>Toll-like receptors</subject><subject>Up-Regulation - drug effects</subject><subject>Water content</subject><issn>1095-6670</issn><issn>1099-0461</issn><issn>1099-0461</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc9u1DAQhy0EomXhwAsgS1zgkMZ_4tg-dgvtLtpCtU3PkZNMNlll48VOqHLjzoXn4SF4CJ4E0205IHGa0eibb0b6IfSSkhNKCIu3xXAiCeHiETqmROuIJCl9fNeLKE0lOULPvN8SQoSW4ik64loIliT6GH27MmB72-HTroMvrRnA4-uxMM6UTW_bCi9gZ51rzAbwst-ObsJtj9dm8DhrnB03Db7ZO9iMnRla22Nb4-vlOqPY9FVYaNqifZgvLi_mNM5W6yS-nN4pFX88__X1-88fc3xlhubWTM_Rk9p0Hl7c1xm6OX-fnS2i1aeL5dnpKipZwkUEtaGaVxwKKRlNOGWqKrWqREVIwhSRpiScaakUYWlVF6LmvAaRgoEyBan4DL05ePfOfh7BD_mu9SV0nenBjj4PRp0qloYrM_T6H3RrR9eH7wIVTmuuJQ3U2wNVOuu9gzrfu3Zn3JRTkv9JKA8J5XcJBfbVvXEsdlD9JR8iCUB8AG7bDqb_m_IP8-yg_A3Ao5oa</recordid><startdate>202412</startdate><enddate>202412</enddate><creator>Liu, Zhao</creator><creator>Zhu, Jun</creator><creator>Pan, Enyu</creator><creator>Pang, Lujun</creator><creator>Zhou, Xiwei</creator><creator>Che, Yanjun</creator><general>Wiley Subscription Services, Inc</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>7QO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0009-0003-3551-8424</orcidid></search><sort><creationdate>202412</creationdate><title>Paeonol Alleviates Subarachnoid Hemorrhage Injury in Rats Through Upregulation of SIRT1 and Inhibition of HMGB1/TLR4/MyD88/NF‐κB Pathway</title><author>Liu, Zhao ; Zhu, Jun ; Pan, Enyu ; Pang, Lujun ; Zhou, Xiwei ; Che, Yanjun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2435-efa193d3eb772143128dc98d5d0042807ac0329788026dfb5f33fe56eaec6e783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acetophenones - pharmacology</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Bioactive compounds</topic><topic>Blood-brain barrier</topic><topic>Blood-Brain Barrier - drug effects</topic><topic>Blood-Brain Barrier - metabolism</topic><topic>Brain injury</topic><topic>Cardiovascular system</topic><topic>Degeneration</topic><topic>Edema</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Extravasation</topic><topic>Head injuries</topic><topic>Hemorrhage</topic><topic>HMGB1</topic><topic>HMGB1 protein</topic><topic>HMGB1 Protein - metabolism</topic><topic>Immunofluorescence</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Inhibitors</topic><topic>Injury analysis</topic><topic>Male</topic><topic>Membrane permeability</topic><topic>Moisture content</topic><topic>MyD88 protein</topic><topic>Myeloid Differentiation Factor 88 - metabolism</topic><topic>Neurodegeneration</topic><topic>Neurological diseases</topic><topic>Neuroprotection</topic><topic>NF-kappa B - metabolism</topic><topic>NF‐κB</topic><topic>paeonol</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Serum levels</topic><topic>Signal Transduction - drug effects</topic><topic>SIRT1</topic><topic>SIRT1 protein</topic><topic>Sirtuin 1 - metabolism</topic><topic>Staining</topic><topic>Stroke</topic><topic>Subarachnoid hemorrhage</topic><topic>Subarachnoid Hemorrhage - drug therapy</topic><topic>Subarachnoid Hemorrhage - metabolism</topic><topic>Subarachnoid Hemorrhage - pathology</topic><topic>TLR4 protein</topic><topic>Toll-Like Receptor 4 - metabolism</topic><topic>Toll-like receptors</topic><topic>Up-Regulation - drug effects</topic><topic>Water content</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Zhao</creatorcontrib><creatorcontrib>Zhu, Jun</creatorcontrib><creatorcontrib>Pan, Enyu</creatorcontrib><creatorcontrib>Pang, Lujun</creatorcontrib><creatorcontrib>Zhou, Xiwei</creatorcontrib><creatorcontrib>Che, Yanjun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of biochemical and molecular toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Zhao</au><au>Zhu, Jun</au><au>Pan, Enyu</au><au>Pang, Lujun</au><au>Zhou, Xiwei</au><au>Che, Yanjun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Paeonol Alleviates Subarachnoid Hemorrhage Injury in Rats Through Upregulation of SIRT1 and Inhibition of HMGB1/TLR4/MyD88/NF‐κB Pathway</atitle><jtitle>Journal of biochemical and molecular toxicology</jtitle><addtitle>J Biochem Mol Toxicol</addtitle><date>2024-12</date><risdate>2024</risdate><volume>38</volume><issue>12</issue><spage>e70035</spage><epage>n/a</epage><pages>e70035-n/a</pages><issn>1095-6670</issn><issn>1099-0461</issn><eissn>1099-0461</eissn><abstract>ABSTRACT
Paeonol is a principle bioactive compound separated from the root bark of Cortex Moutan and has been shown to confer various biological functions, including antineuroinflammation and neuroprotection. Inflammation, blood–brain barrier (BBB), permeability, and apoptosis are three major underlying mechanisms involved in early brain injury (EBI) postsubarachnoid hemorrhage (SAH). This study aimed to detect the roles and mechanisms of paeonol in EBI following SAH. A SAH model was established by an endovascular perforation method in Sprague‐Dawley rats. The localizations of HMGB1 and p65 were identified by immunofluorescence staining. Protein levels were measured by western blot analysis. The serum levels of HMGB1 and the levels of inflammatory cytokines in the brain cortex were evaluated by ELISA. Hematoxylin and eosin staining was conducted to detect neuronal degeneration. Brain water content and Evans blue extravasation were assessed to determine EBI. Neuronal apoptosis was examined by TUNEL. Paeonol deacetylated HMGB1 by upregulating SIRT1 level. SIRT1 inhibition attenuated the protective effects of paeonol against neurological dysfunctions, brain edema, and BBB disruption. SIRT1 inhibition rescued the paeonol‐induced inhibition in inflammatory response. The paeonol‐induced decrease in neuronal apoptosis was restored by SIRT1 inhibitor. The paeonol‐mediated deactivated TLR4/MyD88/NF‐κB pathway was activated by SIRT1 inhibitor. Paeonol alleviates the SAH injury in rats by upregulating SIRT1 to inactivate the HMGB1/TLR4/MyD88/NF‐κB pathway.
Scientific diagram demonstrating the underlying mechanisms involving in neuroprotective effects of paeonol.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>39552449</pmid><doi>10.1002/jbt.70035</doi><tpages>12</tpages><orcidid>https://orcid.org/0009-0003-3551-8424</orcidid></addata></record> |
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| subjects | Acetophenones - pharmacology Animals Apoptosis Apoptosis - drug effects Bioactive compounds Blood-brain barrier Blood-Brain Barrier - drug effects Blood-Brain Barrier - metabolism Brain injury Cardiovascular system Degeneration Edema Enzyme-linked immunosorbent assay Extravasation Head injuries Hemorrhage HMGB1 HMGB1 protein HMGB1 Protein - metabolism Immunofluorescence Inflammation Inflammatory response Inhibitors Injury analysis Male Membrane permeability Moisture content MyD88 protein Myeloid Differentiation Factor 88 - metabolism Neurodegeneration Neurological diseases Neuroprotection NF-kappa B - metabolism NF‐κB paeonol Rats Rats, Sprague-Dawley Serum levels Signal Transduction - drug effects SIRT1 SIRT1 protein Sirtuin 1 - metabolism Staining Stroke Subarachnoid hemorrhage Subarachnoid Hemorrhage - drug therapy Subarachnoid Hemorrhage - metabolism Subarachnoid Hemorrhage - pathology TLR4 protein Toll-Like Receptor 4 - metabolism Toll-like receptors Up-Regulation - drug effects Water content |
| title | Paeonol Alleviates Subarachnoid Hemorrhage Injury in Rats Through Upregulation of SIRT1 and Inhibition of HMGB1/TLR4/MyD88/NF‐κB Pathway |
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