Zhilong Huoxue Tongyu Capsule regulates the macrophage polarization and inflammatory response via the let-7i/TLR9/MyD88 signaling pathway
Zhilong Huoxue Tongyu Capsule (ZL) is clinically prescribed for acute ischemic stroke (AIS). However, only a few studies have addressed the mechanisms of ZL in treating AIS. To explore the underlying mechanism of macrophage polarization and inflammation mediated by ZL, and to provide a reference for...
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| Veröffentlicht in: | Journal of ethnopharmacology 2024-08, Vol.330, p.118208-118208, Article 118208 |
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| creator | Kang, Ya-Fei Bai, Xue Wang, Kong-Yu Wang, Tao Pan, Chuan-Ling Xie, Cheng Liang, Bo Liao, Hui-Ling |
| description | Zhilong Huoxue Tongyu Capsule (ZL) is clinically prescribed for acute ischemic stroke (AIS). However, only a few studies have addressed the mechanisms of ZL in treating AIS.
To explore the underlying mechanism of macrophage polarization and inflammation mediated by ZL, and to provide a reference for AIS treatment.
Sixteen SD rats were fed with different dose of ZL (0, 0.4, 0.8, and 1.6 g/kg/d) for 4 days to prepare ZL serum. After 500 ng/mL lipopolysaccharide (LPS) stimulation, RAW264.7 cells were administrated with ZL serum. Then, experiments including ELISA, flow cytometry, real-time quantitative PCR and Western blot were performed to verify the effects of ZL on macrophage polarization and inflammation. Next, let-7i inhibitor was transfected in RAW264.7 cells when treated with LPS and ZL serum to verify the regulation of ZL on the let-7i/TLR9/MyD88 signaling pathway. Moreover, the interaction between let-7i and TLR9 was confirmed by the dual-luciferase assay.
ZL serum significantly decreased the expression of interleukin (IL)-6 and tumor necrosis factor-α (TNF-α), and increased the expression of IL-10 and transforming growth factor β1 (TGF-β1) of LPS stimulated-macrophages. Furthermore, ZL serum polarized macrophages toward M2, decreased the expressions of TLR9, MyD88, and iNOS, as well as increased the expressions of let-7i, CHIL3, and Arginase-1. It is worth mentioning that the effect of ZL serum is dose-dependent. However, let-7i inhibitor restored all the above effects in LPS stimulated-macrophages. In addition, TLR9 was the target of let-7i.
ZL targeted let-7i to inhibit TLR9 expression, thereby inhibiting the activation of the TLR9/MyD88 pathway, promoting the M2 polarization, and inhibiting the development of inflammation in AIS.
[Display omitted]
•ZL is clinically prescribed for AIS.•ZL promotes M2 polarization and inhibited inflammation.•ZL targetes let-7i to inhibit the TLR9/MyD88 pathway. |
| doi_str_mv | 10.1016/j.jep.2024.118208 |
| format | Article |
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To explore the underlying mechanism of macrophage polarization and inflammation mediated by ZL, and to provide a reference for AIS treatment.
Sixteen SD rats were fed with different dose of ZL (0, 0.4, 0.8, and 1.6 g/kg/d) for 4 days to prepare ZL serum. After 500 ng/mL lipopolysaccharide (LPS) stimulation, RAW264.7 cells were administrated with ZL serum. Then, experiments including ELISA, flow cytometry, real-time quantitative PCR and Western blot were performed to verify the effects of ZL on macrophage polarization and inflammation. Next, let-7i inhibitor was transfected in RAW264.7 cells when treated with LPS and ZL serum to verify the regulation of ZL on the let-7i/TLR9/MyD88 signaling pathway. Moreover, the interaction between let-7i and TLR9 was confirmed by the dual-luciferase assay.
ZL serum significantly decreased the expression of interleukin (IL)-6 and tumor necrosis factor-α (TNF-α), and increased the expression of IL-10 and transforming growth factor β1 (TGF-β1) of LPS stimulated-macrophages. Furthermore, ZL serum polarized macrophages toward M2, decreased the expressions of TLR9, MyD88, and iNOS, as well as increased the expressions of let-7i, CHIL3, and Arginase-1. It is worth mentioning that the effect of ZL serum is dose-dependent. However, let-7i inhibitor restored all the above effects in LPS stimulated-macrophages. In addition, TLR9 was the target of let-7i.
ZL targeted let-7i to inhibit TLR9 expression, thereby inhibiting the activation of the TLR9/MyD88 pathway, promoting the M2 polarization, and inhibiting the development of inflammation in AIS.
[Display omitted]
•ZL is clinically prescribed for AIS.•ZL promotes M2 polarization and inhibited inflammation.•ZL targetes let-7i to inhibit the TLR9/MyD88 pathway.</description><identifier>ISSN: 0378-8741</identifier><identifier>EISSN: 1872-7573</identifier><identifier>DOI: 10.1016/j.jep.2024.118208</identifier><identifier>PMID: 38636581</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Acute ischemic stroke ; blood serum ; dose response ; flow cytometry ; Inflammation ; interleukin-10 ; Let-7i ; lipopolysaccharides ; M2 polarization ; macrophages ; necrosis ; neoplasms ; quantitative polymerase chain reaction ; stroke ; TLR9/MyD88 signaling pathway ; Traditional Chinese medicine ; traditional medicine ; Western blotting ; Zhilong huoxue tongyu capsule</subject><ispartof>Journal of ethnopharmacology, 2024-08, Vol.330, p.118208-118208, Article 118208</ispartof><rights>2024 Elsevier B.V.</rights><rights>Copyright © 2024. Published by Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c338t-88194e63a8b5619ee4c04c0ff55a9910300b18fd77b02edc16a88c30843bf0223</cites><orcidid>0000-0002-1749-6976</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0378874124005075$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38636581$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kang, Ya-Fei</creatorcontrib><creatorcontrib>Bai, Xue</creatorcontrib><creatorcontrib>Wang, Kong-Yu</creatorcontrib><creatorcontrib>Wang, Tao</creatorcontrib><creatorcontrib>Pan, Chuan-Ling</creatorcontrib><creatorcontrib>Xie, Cheng</creatorcontrib><creatorcontrib>Liang, Bo</creatorcontrib><creatorcontrib>Liao, Hui-Ling</creatorcontrib><title>Zhilong Huoxue Tongyu Capsule regulates the macrophage polarization and inflammatory response via the let-7i/TLR9/MyD88 signaling pathway</title><title>Journal of ethnopharmacology</title><addtitle>J Ethnopharmacol</addtitle><description>Zhilong Huoxue Tongyu Capsule (ZL) is clinically prescribed for acute ischemic stroke (AIS). However, only a few studies have addressed the mechanisms of ZL in treating AIS.
To explore the underlying mechanism of macrophage polarization and inflammation mediated by ZL, and to provide a reference for AIS treatment.
Sixteen SD rats were fed with different dose of ZL (0, 0.4, 0.8, and 1.6 g/kg/d) for 4 days to prepare ZL serum. After 500 ng/mL lipopolysaccharide (LPS) stimulation, RAW264.7 cells were administrated with ZL serum. Then, experiments including ELISA, flow cytometry, real-time quantitative PCR and Western blot were performed to verify the effects of ZL on macrophage polarization and inflammation. Next, let-7i inhibitor was transfected in RAW264.7 cells when treated with LPS and ZL serum to verify the regulation of ZL on the let-7i/TLR9/MyD88 signaling pathway. Moreover, the interaction between let-7i and TLR9 was confirmed by the dual-luciferase assay.
ZL serum significantly decreased the expression of interleukin (IL)-6 and tumor necrosis factor-α (TNF-α), and increased the expression of IL-10 and transforming growth factor β1 (TGF-β1) of LPS stimulated-macrophages. Furthermore, ZL serum polarized macrophages toward M2, decreased the expressions of TLR9, MyD88, and iNOS, as well as increased the expressions of let-7i, CHIL3, and Arginase-1. It is worth mentioning that the effect of ZL serum is dose-dependent. However, let-7i inhibitor restored all the above effects in LPS stimulated-macrophages. In addition, TLR9 was the target of let-7i.
ZL targeted let-7i to inhibit TLR9 expression, thereby inhibiting the activation of the TLR9/MyD88 pathway, promoting the M2 polarization, and inhibiting the development of inflammation in AIS.
[Display omitted]
•ZL is clinically prescribed for AIS.•ZL promotes M2 polarization and inhibited inflammation.•ZL targetes let-7i to inhibit the TLR9/MyD88 pathway.</description><subject>Acute ischemic stroke</subject><subject>blood serum</subject><subject>dose response</subject><subject>flow cytometry</subject><subject>Inflammation</subject><subject>interleukin-10</subject><subject>Let-7i</subject><subject>lipopolysaccharides</subject><subject>M2 polarization</subject><subject>macrophages</subject><subject>necrosis</subject><subject>neoplasms</subject><subject>quantitative polymerase chain reaction</subject><subject>stroke</subject><subject>TLR9/MyD88 signaling pathway</subject><subject>Traditional Chinese medicine</subject><subject>traditional medicine</subject><subject>Western blotting</subject><subject>Zhilong huoxue tongyu capsule</subject><issn>0378-8741</issn><issn>1872-7573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNqFkcGO0zAQhi0EYsvCA3BBPnJJa8dO7IgT6gKLVISEyoWLNUkmrSsnDnaykH2DfWu8dOEIkqXx4fv_keYj5CVna854uTmtTziuc5bLNec6Z_oRWXGt8kwVSjwmKyaUzrSS_II8i_HEGFNcsqfkQuhSlIXmK3L37WidHw70evY_Z6T79F9muoUxzg5pwMPsYMJIpyPSHprgxyMckI7eQbC3MFk_UBhaaofOQd_D5MOSYnH0Q0R6Y-F30uGUKbvZ775Um0_LldY02sMAzqbNI0zHH7A8J086cBFfPMxL8vX9u_32Ott9_vBx-3aXNULoKdOaVxJLAbouSl4hyoal13VFAVXFmWCs5rprlapZjm3DS9C6EUxLUXcsz8UleX3uHYP_PmOcTG9jg87BgH6ORvBCKClVqvovyqRgqpBVmVB-RtOFYgzYmTHYHsJiODP3sszJJFnmXpY5y0qZVw_1c91j-zfxx04C3pwBTPe4sRhMbCwODbY2YDOZ1tt_1P8C4kylaQ</recordid><startdate>20240810</startdate><enddate>20240810</enddate><creator>Kang, Ya-Fei</creator><creator>Bai, Xue</creator><creator>Wang, Kong-Yu</creator><creator>Wang, Tao</creator><creator>Pan, Chuan-Ling</creator><creator>Xie, Cheng</creator><creator>Liang, Bo</creator><creator>Liao, Hui-Ling</creator><general>Elsevier B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0002-1749-6976</orcidid></search><sort><creationdate>20240810</creationdate><title>Zhilong Huoxue Tongyu Capsule regulates the macrophage polarization and inflammatory response via the let-7i/TLR9/MyD88 signaling pathway</title><author>Kang, Ya-Fei ; Bai, Xue ; Wang, Kong-Yu ; Wang, Tao ; Pan, Chuan-Ling ; Xie, Cheng ; Liang, Bo ; Liao, Hui-Ling</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c338t-88194e63a8b5619ee4c04c0ff55a9910300b18fd77b02edc16a88c30843bf0223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acute ischemic stroke</topic><topic>blood serum</topic><topic>dose response</topic><topic>flow cytometry</topic><topic>Inflammation</topic><topic>interleukin-10</topic><topic>Let-7i</topic><topic>lipopolysaccharides</topic><topic>M2 polarization</topic><topic>macrophages</topic><topic>necrosis</topic><topic>neoplasms</topic><topic>quantitative polymerase chain reaction</topic><topic>stroke</topic><topic>TLR9/MyD88 signaling pathway</topic><topic>Traditional Chinese medicine</topic><topic>traditional medicine</topic><topic>Western blotting</topic><topic>Zhilong huoxue tongyu capsule</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kang, Ya-Fei</creatorcontrib><creatorcontrib>Bai, Xue</creatorcontrib><creatorcontrib>Wang, Kong-Yu</creatorcontrib><creatorcontrib>Wang, Tao</creatorcontrib><creatorcontrib>Pan, Chuan-Ling</creatorcontrib><creatorcontrib>Xie, Cheng</creatorcontrib><creatorcontrib>Liang, Bo</creatorcontrib><creatorcontrib>Liao, Hui-Ling</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Journal of ethnopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kang, Ya-Fei</au><au>Bai, Xue</au><au>Wang, Kong-Yu</au><au>Wang, Tao</au><au>Pan, Chuan-Ling</au><au>Xie, Cheng</au><au>Liang, Bo</au><au>Liao, Hui-Ling</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Zhilong Huoxue Tongyu Capsule regulates the macrophage polarization and inflammatory response via the let-7i/TLR9/MyD88 signaling pathway</atitle><jtitle>Journal of ethnopharmacology</jtitle><addtitle>J Ethnopharmacol</addtitle><date>2024-08-10</date><risdate>2024</risdate><volume>330</volume><spage>118208</spage><epage>118208</epage><pages>118208-118208</pages><artnum>118208</artnum><issn>0378-8741</issn><eissn>1872-7573</eissn><abstract>Zhilong Huoxue Tongyu Capsule (ZL) is clinically prescribed for acute ischemic stroke (AIS). However, only a few studies have addressed the mechanisms of ZL in treating AIS.
To explore the underlying mechanism of macrophage polarization and inflammation mediated by ZL, and to provide a reference for AIS treatment.
Sixteen SD rats were fed with different dose of ZL (0, 0.4, 0.8, and 1.6 g/kg/d) for 4 days to prepare ZL serum. After 500 ng/mL lipopolysaccharide (LPS) stimulation, RAW264.7 cells were administrated with ZL serum. Then, experiments including ELISA, flow cytometry, real-time quantitative PCR and Western blot were performed to verify the effects of ZL on macrophage polarization and inflammation. Next, let-7i inhibitor was transfected in RAW264.7 cells when treated with LPS and ZL serum to verify the regulation of ZL on the let-7i/TLR9/MyD88 signaling pathway. Moreover, the interaction between let-7i and TLR9 was confirmed by the dual-luciferase assay.
ZL serum significantly decreased the expression of interleukin (IL)-6 and tumor necrosis factor-α (TNF-α), and increased the expression of IL-10 and transforming growth factor β1 (TGF-β1) of LPS stimulated-macrophages. Furthermore, ZL serum polarized macrophages toward M2, decreased the expressions of TLR9, MyD88, and iNOS, as well as increased the expressions of let-7i, CHIL3, and Arginase-1. It is worth mentioning that the effect of ZL serum is dose-dependent. However, let-7i inhibitor restored all the above effects in LPS stimulated-macrophages. In addition, TLR9 was the target of let-7i.
ZL targeted let-7i to inhibit TLR9 expression, thereby inhibiting the activation of the TLR9/MyD88 pathway, promoting the M2 polarization, and inhibiting the development of inflammation in AIS.
[Display omitted]
•ZL is clinically prescribed for AIS.•ZL promotes M2 polarization and inhibited inflammation.•ZL targetes let-7i to inhibit the TLR9/MyD88 pathway.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>38636581</pmid><doi>10.1016/j.jep.2024.118208</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-1749-6976</orcidid></addata></record> |
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| source | Elsevier ScienceDirect Journals |
| subjects | Acute ischemic stroke blood serum dose response flow cytometry Inflammation interleukin-10 Let-7i lipopolysaccharides M2 polarization macrophages necrosis neoplasms quantitative polymerase chain reaction stroke TLR9/MyD88 signaling pathway Traditional Chinese medicine traditional medicine Western blotting Zhilong huoxue tongyu capsule |
| title | Zhilong Huoxue Tongyu Capsule regulates the macrophage polarization and inflammatory response via the let-7i/TLR9/MyD88 signaling pathway |
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