Salvianolic acid A alleviated inflammatory response mediated by microglia through inhibiting the activation of TLR2/4 in acute cerebral ischemia-reperfusion
•Salvianolic acid A (SAA) improves cerebral ischemia-reperfusion injury in SD rats•SAA inhibits TLR2 and TLR4 expression in ischemic brain tissue•SAA ameliorates oxygen glucose deprivation injury in primary microglia•SAA inhibits microglial mediated inflammation via MyD88 dependent TLR2/4 pathway To...
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| creator | Ling, Yun Jin, Lu Ma, Quanxin Huang, Yu Yang, Qinqin Chen, Minli Shou, Qiyang |
| description | •Salvianolic acid A (SAA) improves cerebral ischemia-reperfusion injury in SD rats•SAA inhibits TLR2 and TLR4 expression in ischemic brain tissue•SAA ameliorates oxygen glucose deprivation injury in primary microglia•SAA inhibits microglial mediated inflammation via MyD88 dependent TLR2/4 pathway
Toll-like receptor 2 and Toll-like receptor 4 (TLR2/4) on microglia have been found as important regulators in the inflammatory response during cerebral ischemia/reperfusion (I/R). In China, traditional Chinese medicine Salvia miltiorrhiza (danshen) and its some components are considered to be effective in rescuing cerebral I/R injury through clinical practice.
Here we examined the effect of Salvianolic acid A (SAA), a monomer compound in the water extract of Salvia miltiorrhiza, on TLR2/4 of microglia and its mediated inflammatory injury during cerebral I/R in vivo and in vitro.
For exploring the effect of SAA on cerebral I/R and TLR2/4, classic middle cerebral artery occlusion (MCAO) model and oxygen glucose deprivation / reoxygenation (OGD/R) model of co-culture with primary hippocampal neurons and microglia in vitro were used. Signal pathway research and gene knockout have been applied to further explain its mechanism.
The evaluation indexes of I/R injury included infarct size, edema degree and pathology as well as primary hippocampal neurons and microglia culture, ELISA, western, RT-PCR, HE staining, immunofluorescence, flow cytometry, siRNA gene knockout were also employed.
SAA significantly improved the degree of brain edema and ischemic area in I/R rats accompanied by decreases in levels of interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α). Pathological staining revealed that SAA could reduce inflammatory cell infiltration and mcirogila activation after reperfusion. Both protein and gene expression of TLR2 and TLR4 in ischemic hemisphere were obviously inhibited by SAA treatment while changes were not found in the non-ischemic hemisphere. In order to further study its mechanism, OGD/R model was used to mimic inflammatory damage of ischemic tissue by co-culturing primary rat hippocampal neurons and microglial cells. It was found that SAA also inhibited the protein and gene expression of TLR2 and TLR4 after OGD/R injury in microglia. After TLR2/4 knockout, the inhibitory effect of SAA on IL-1β and TNF-α levels in cell supernatant and neuron apoptosis were significantly weakened in each dose group. Moreover, expression levels of myeloid different |
| doi_str_mv | 10.1016/j.phymed.2021.153569 |
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Toll-like receptor 2 and Toll-like receptor 4 (TLR2/4) on microglia have been found as important regulators in the inflammatory response during cerebral ischemia/reperfusion (I/R). In China, traditional Chinese medicine Salvia miltiorrhiza (danshen) and its some components are considered to be effective in rescuing cerebral I/R injury through clinical practice.
Here we examined the effect of Salvianolic acid A (SAA), a monomer compound in the water extract of Salvia miltiorrhiza, on TLR2/4 of microglia and its mediated inflammatory injury during cerebral I/R in vivo and in vitro.
For exploring the effect of SAA on cerebral I/R and TLR2/4, classic middle cerebral artery occlusion (MCAO) model and oxygen glucose deprivation / reoxygenation (OGD/R) model of co-culture with primary hippocampal neurons and microglia in vitro were used. Signal pathway research and gene knockout have been applied to further explain its mechanism.
The evaluation indexes of I/R injury included infarct size, edema degree and pathology as well as primary hippocampal neurons and microglia culture, ELISA, western, RT-PCR, HE staining, immunofluorescence, flow cytometry, siRNA gene knockout were also employed.
SAA significantly improved the degree of brain edema and ischemic area in I/R rats accompanied by decreases in levels of interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α). Pathological staining revealed that SAA could reduce inflammatory cell infiltration and mcirogila activation after reperfusion. Both protein and gene expression of TLR2 and TLR4 in ischemic hemisphere were obviously inhibited by SAA treatment while changes were not found in the non-ischemic hemisphere. In order to further study its mechanism, OGD/R model was used to mimic inflammatory damage of ischemic tissue by co-culturing primary rat hippocampal neurons and microglial cells. It was found that SAA also inhibited the protein and gene expression of TLR2 and TLR4 after OGD/R injury in microglia. After TLR2/4 knockout, the inhibitory effect of SAA on IL-1β and TNF-α levels in cell supernatant and neuron apoptosis were significantly weakened in each dose group. Moreover, expression levels of myeloid differentiation factor 88 (MyD88), NFκB, IL-1β and IL-6 in TLR2/4 mediated inflammatory pathway were reduced with SAA treatment.
SAA could significantly reduce the inflammatory response and injury in cerebral ischemia-reperfusion in vivo and in vitro, and its mechanism may be through the inhibition of TLR2/4 and its related signal pathway.
[Display omitted]</description><identifier>ISSN: 0944-7113</identifier><identifier>EISSN: 1618-095X</identifier><identifier>DOI: 10.1016/j.phymed.2021.153569</identifier><identifier>PMID: 33985878</identifier><language>eng</language><publisher>Germany: Elsevier GmbH</publisher><subject>Animals ; Brain Ischemia - drug therapy ; Brain Ischemia - pathology ; Caffeic Acids - pharmacology ; Caffeic Acids - therapeutic use ; Infarction, Middle Cerebral Artery ; inflammation ; Inflammation - metabolism ; Lactates - pharmacology ; Lactates - therapeutic use ; Male ; Microglia ; Microglia - drug effects ; Microglia - metabolism ; Myeloid Differentiation Factor 88 - metabolism ; NF-kappa B - metabolism ; Rats ; Reperfusion Injury - drug therapy ; Salvianolic acid A ; Signal Transduction - drug effects ; Toll-like receptor 2 ; Toll-Like Receptor 2 - antagonists & inhibitors ; Toll-Like Receptor 2 - genetics ; Toll-Like Receptor 2 - metabolism ; Toll-like receptor 4 ; Toll-Like Receptor 4 - antagonists & inhibitors ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - metabolism</subject><ispartof>Phytomedicine (Stuttgart), 2021-07, Vol.87, p.153569-153569, Article 153569</ispartof><rights>2021</rights><rights>Copyright © 2021. Published by Elsevier GmbH.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-52e212f14d13a961352dd1fb87c71fbd22c271c871bdbfd6d057ebb362d023113</citedby><cites>FETCH-LOGICAL-c362t-52e212f14d13a961352dd1fb87c71fbd22c271c871bdbfd6d057ebb362d023113</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0944711321001112$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33985878$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ling, Yun</creatorcontrib><creatorcontrib>Jin, Lu</creatorcontrib><creatorcontrib>Ma, Quanxin</creatorcontrib><creatorcontrib>Huang, Yu</creatorcontrib><creatorcontrib>Yang, Qinqin</creatorcontrib><creatorcontrib>Chen, Minli</creatorcontrib><creatorcontrib>Shou, Qiyang</creatorcontrib><title>Salvianolic acid A alleviated inflammatory response mediated by microglia through inhibiting the activation of TLR2/4 in acute cerebral ischemia-reperfusion</title><title>Phytomedicine (Stuttgart)</title><addtitle>Phytomedicine</addtitle><description>•Salvianolic acid A (SAA) improves cerebral ischemia-reperfusion injury in SD rats•SAA inhibits TLR2 and TLR4 expression in ischemic brain tissue•SAA ameliorates oxygen glucose deprivation injury in primary microglia•SAA inhibits microglial mediated inflammation via MyD88 dependent TLR2/4 pathway
Toll-like receptor 2 and Toll-like receptor 4 (TLR2/4) on microglia have been found as important regulators in the inflammatory response during cerebral ischemia/reperfusion (I/R). In China, traditional Chinese medicine Salvia miltiorrhiza (danshen) and its some components are considered to be effective in rescuing cerebral I/R injury through clinical practice.
Here we examined the effect of Salvianolic acid A (SAA), a monomer compound in the water extract of Salvia miltiorrhiza, on TLR2/4 of microglia and its mediated inflammatory injury during cerebral I/R in vivo and in vitro.
For exploring the effect of SAA on cerebral I/R and TLR2/4, classic middle cerebral artery occlusion (MCAO) model and oxygen glucose deprivation / reoxygenation (OGD/R) model of co-culture with primary hippocampal neurons and microglia in vitro were used. Signal pathway research and gene knockout have been applied to further explain its mechanism.
The evaluation indexes of I/R injury included infarct size, edema degree and pathology as well as primary hippocampal neurons and microglia culture, ELISA, western, RT-PCR, HE staining, immunofluorescence, flow cytometry, siRNA gene knockout were also employed.
SAA significantly improved the degree of brain edema and ischemic area in I/R rats accompanied by decreases in levels of interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α). Pathological staining revealed that SAA could reduce inflammatory cell infiltration and mcirogila activation after reperfusion. Both protein and gene expression of TLR2 and TLR4 in ischemic hemisphere were obviously inhibited by SAA treatment while changes were not found in the non-ischemic hemisphere. In order to further study its mechanism, OGD/R model was used to mimic inflammatory damage of ischemic tissue by co-culturing primary rat hippocampal neurons and microglial cells. It was found that SAA also inhibited the protein and gene expression of TLR2 and TLR4 after OGD/R injury in microglia. After TLR2/4 knockout, the inhibitory effect of SAA on IL-1β and TNF-α levels in cell supernatant and neuron apoptosis were significantly weakened in each dose group. Moreover, expression levels of myeloid differentiation factor 88 (MyD88), NFκB, IL-1β and IL-6 in TLR2/4 mediated inflammatory pathway were reduced with SAA treatment.
SAA could significantly reduce the inflammatory response and injury in cerebral ischemia-reperfusion in vivo and in vitro, and its mechanism may be through the inhibition of TLR2/4 and its related signal pathway.
[Display omitted]</description><subject>Animals</subject><subject>Brain Ischemia - drug therapy</subject><subject>Brain Ischemia - pathology</subject><subject>Caffeic Acids - pharmacology</subject><subject>Caffeic Acids - therapeutic use</subject><subject>Infarction, Middle Cerebral Artery</subject><subject>inflammation</subject><subject>Inflammation - metabolism</subject><subject>Lactates - pharmacology</subject><subject>Lactates - therapeutic use</subject><subject>Male</subject><subject>Microglia</subject><subject>Microglia - drug effects</subject><subject>Microglia - metabolism</subject><subject>Myeloid Differentiation Factor 88 - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Rats</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Salvianolic acid A</subject><subject>Signal Transduction - drug effects</subject><subject>Toll-like receptor 2</subject><subject>Toll-Like Receptor 2 - antagonists & inhibitors</subject><subject>Toll-Like Receptor 2 - genetics</subject><subject>Toll-Like Receptor 2 - metabolism</subject><subject>Toll-like receptor 4</subject><subject>Toll-Like Receptor 4 - antagonists & inhibitors</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - metabolism</subject><issn>0944-7113</issn><issn>1618-095X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UU1r3DAQFaWl2aT9B6Xo2Is3Gvn7UgghbQMLhSaB3IQsjddaZMuV5IX9L_2x0eLkWnQYePPePM08Qr4A2wKD6vqwnYfTiHrLGYctlHlZte_IBipoMtaWz-_JhrVFkdUA-QW5DOHAGBRtzT6Sizxvm7Kpmw359yDt0cjJWaOoVEbTGyqtxYRF1NRMvZXjKKPzJ-oxzG4KSJPr2u5OdDTKu701ksbBu2U_JM1gOhPNtE8QpqHRHGU0bqKup4-7P_y6SJyELxGpQo-dl5aaoAYcjcw8zuj7JSTBJ_Khlzbg59d6RZ5-3D3e_sp2v3_e397sMpVXPGYlRw68h0JDLtsK8pJrDX3X1KpORXOueA2qqaHTXa8rzcoauy5pNeN5Os8V-bbOnb37u2CIYkzfQWvlhG4Jgpe8gfOrErVYqWnrEDz2YvZmlP4kgIlzLuIg1lzEORex5pJkX18dlu7cexO9BZEI31cCpj2PBr0IyuCk0qU9qii0M_93eAEKXqPC</recordid><startdate>202107</startdate><enddate>202107</enddate><creator>Ling, Yun</creator><creator>Jin, Lu</creator><creator>Ma, Quanxin</creator><creator>Huang, Yu</creator><creator>Yang, Qinqin</creator><creator>Chen, Minli</creator><creator>Shou, Qiyang</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></search><sort><creationdate>202107</creationdate><title>Salvianolic acid A alleviated inflammatory response mediated by microglia through inhibiting the activation of TLR2/4 in acute cerebral ischemia-reperfusion</title><author>Ling, Yun ; Jin, Lu ; Ma, Quanxin ; Huang, Yu ; Yang, Qinqin ; Chen, Minli ; Shou, Qiyang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-52e212f14d13a961352dd1fb87c71fbd22c271c871bdbfd6d057ebb362d023113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Brain Ischemia - drug therapy</topic><topic>Brain Ischemia - pathology</topic><topic>Caffeic Acids - pharmacology</topic><topic>Caffeic Acids - therapeutic use</topic><topic>Infarction, Middle Cerebral Artery</topic><topic>inflammation</topic><topic>Inflammation - metabolism</topic><topic>Lactates - pharmacology</topic><topic>Lactates - therapeutic use</topic><topic>Male</topic><topic>Microglia</topic><topic>Microglia - drug effects</topic><topic>Microglia - metabolism</topic><topic>Myeloid Differentiation Factor 88 - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Rats</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Salvianolic acid A</topic><topic>Signal Transduction - drug effects</topic><topic>Toll-like receptor 2</topic><topic>Toll-Like Receptor 2 - antagonists & inhibitors</topic><topic>Toll-Like Receptor 2 - genetics</topic><topic>Toll-Like Receptor 2 - metabolism</topic><topic>Toll-like receptor 4</topic><topic>Toll-Like Receptor 4 - antagonists & inhibitors</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-Like Receptor 4 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ling, Yun</creatorcontrib><creatorcontrib>Jin, Lu</creatorcontrib><creatorcontrib>Ma, Quanxin</creatorcontrib><creatorcontrib>Huang, Yu</creatorcontrib><creatorcontrib>Yang, Qinqin</creatorcontrib><creatorcontrib>Chen, Minli</creatorcontrib><creatorcontrib>Shou, Qiyang</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><jtitle>Phytomedicine (Stuttgart)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ling, Yun</au><au>Jin, Lu</au><au>Ma, Quanxin</au><au>Huang, Yu</au><au>Yang, Qinqin</au><au>Chen, Minli</au><au>Shou, Qiyang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Salvianolic acid A alleviated inflammatory response mediated by microglia through inhibiting the activation of TLR2/4 in acute cerebral ischemia-reperfusion</atitle><jtitle>Phytomedicine (Stuttgart)</jtitle><addtitle>Phytomedicine</addtitle><date>2021-07</date><risdate>2021</risdate><volume>87</volume><spage>153569</spage><epage>153569</epage><pages>153569-153569</pages><artnum>153569</artnum><issn>0944-7113</issn><eissn>1618-095X</eissn><abstract>•Salvianolic acid A (SAA) improves cerebral ischemia-reperfusion injury in SD rats•SAA inhibits TLR2 and TLR4 expression in ischemic brain tissue•SAA ameliorates oxygen glucose deprivation injury in primary microglia•SAA inhibits microglial mediated inflammation via MyD88 dependent TLR2/4 pathway
Toll-like receptor 2 and Toll-like receptor 4 (TLR2/4) on microglia have been found as important regulators in the inflammatory response during cerebral ischemia/reperfusion (I/R). In China, traditional Chinese medicine Salvia miltiorrhiza (danshen) and its some components are considered to be effective in rescuing cerebral I/R injury through clinical practice.
Here we examined the effect of Salvianolic acid A (SAA), a monomer compound in the water extract of Salvia miltiorrhiza, on TLR2/4 of microglia and its mediated inflammatory injury during cerebral I/R in vivo and in vitro.
For exploring the effect of SAA on cerebral I/R and TLR2/4, classic middle cerebral artery occlusion (MCAO) model and oxygen glucose deprivation / reoxygenation (OGD/R) model of co-culture with primary hippocampal neurons and microglia in vitro were used. Signal pathway research and gene knockout have been applied to further explain its mechanism.
The evaluation indexes of I/R injury included infarct size, edema degree and pathology as well as primary hippocampal neurons and microglia culture, ELISA, western, RT-PCR, HE staining, immunofluorescence, flow cytometry, siRNA gene knockout were also employed.
SAA significantly improved the degree of brain edema and ischemic area in I/R rats accompanied by decreases in levels of interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α). Pathological staining revealed that SAA could reduce inflammatory cell infiltration and mcirogila activation after reperfusion. Both protein and gene expression of TLR2 and TLR4 in ischemic hemisphere were obviously inhibited by SAA treatment while changes were not found in the non-ischemic hemisphere. In order to further study its mechanism, OGD/R model was used to mimic inflammatory damage of ischemic tissue by co-culturing primary rat hippocampal neurons and microglial cells. It was found that SAA also inhibited the protein and gene expression of TLR2 and TLR4 after OGD/R injury in microglia. After TLR2/4 knockout, the inhibitory effect of SAA on IL-1β and TNF-α levels in cell supernatant and neuron apoptosis were significantly weakened in each dose group. Moreover, expression levels of myeloid differentiation factor 88 (MyD88), NFκB, IL-1β and IL-6 in TLR2/4 mediated inflammatory pathway were reduced with SAA treatment.
SAA could significantly reduce the inflammatory response and injury in cerebral ischemia-reperfusion in vivo and in vitro, and its mechanism may be through the inhibition of TLR2/4 and its related signal pathway.
[Display omitted]</abstract><cop>Germany</cop><pub>Elsevier GmbH</pub><pmid>33985878</pmid><doi>10.1016/j.phymed.2021.153569</doi><tpages>1</tpages></addata></record> |
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| subjects | Animals Brain Ischemia - drug therapy Brain Ischemia - pathology Caffeic Acids - pharmacology Caffeic Acids - therapeutic use Infarction, Middle Cerebral Artery inflammation Inflammation - metabolism Lactates - pharmacology Lactates - therapeutic use Male Microglia Microglia - drug effects Microglia - metabolism Myeloid Differentiation Factor 88 - metabolism NF-kappa B - metabolism Rats Reperfusion Injury - drug therapy Salvianolic acid A Signal Transduction - drug effects Toll-like receptor 2 Toll-Like Receptor 2 - antagonists & inhibitors Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - metabolism Toll-like receptor 4 Toll-Like Receptor 4 - antagonists & inhibitors Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - metabolism |
| title | Salvianolic acid A alleviated inflammatory response mediated by microglia through inhibiting the activation of TLR2/4 in acute cerebral ischemia-reperfusion |
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