Longdan Xiegan decoction ameliorates vulvovaginal candidiasis by inhibiting the NLRP3 inflammasome via the Toll-like receptor /MyD88 pathway

Longdan Xiegan decoction (LXD) is a standardized herbal prescription originally documented in the “Medical Formula Collection” by the eminent physician Wang Ang during the Qing dynasty. It has been used extensively to treat vulvovaginal candidiasis (VVC). However, despite its effectiveness, the mech...

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Veröffentlicht in:Journal of ethnopharmacology 2024-01, Vol.318 (Pt A), p.116869-116869, Article 116869
Hauptverfasser: Feng, Xin, Zhang, Hao, Hu, Kaifan, Shi, Gaoxiang, Wu, Daqiang, Shao, Jing, Wang, Tianming, Wang, Changzhong
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container_issue Pt A
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container_title Journal of ethnopharmacology
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Zhang, Hao
Hu, Kaifan
Shi, Gaoxiang
Wu, Daqiang
Shao, Jing
Wang, Tianming
Wang, Changzhong
description Longdan Xiegan decoction (LXD) is a standardized herbal prescription originally documented in the “Medical Formula Collection” by the eminent physician Wang Ang during the Qing dynasty. It has been used extensively to treat vulvovaginal candidiasis (VVC). However, despite its effectiveness, the mechanism of action remains unknown. To elucidate the mechanism by which LXD relieves VVC via the Toll-like receptor/MyD88 pathway and activation of the NLRP3 inflammasome. Female Kunming mice (n = 96) were randomly divided into six groups: control, VVC model, LXD (10/20/40 mL/kg), and positive drug fluconazole. Mice were vaginally administered Candida albicans (C. albicans) solution (20 μL; 1 × 108 colony-forming units/mL), suspended for 5 min, and observed daily for changes in their condition. Continuous dilution was used to determine the number of colony-forming units. Gram, periodic acid-Schiff, Papanicolaou, and hematoxylin and eosin staining were used to determine the extent of infection. Enzyme-linked immunosorbent assay(ELISA) was used to determine the levels of proinflammatory cytokines IL-1β and IL-18. TLR2, TLR4, MyD88, NF-κB, NLRP3, ASC, and caspase-1 protein expression were determined using western blotting. C. albicans infection destroyed the integrity of the vaginal mucosa, increased fungal burden and the influx of neutrophils into the vaginal cavity, and promoted the secretion of proinflammatory cytokines. C. albicans stimulated the expression of TLR2, TLR4, MyD88, NF-κB, NLRP3, ASC, and caspase-1 in vaginal tissue. Fungal burden, hyphal formation, and C. albicans adhesion were reduced in the 20 and 40 mL/kg LXD groups. Hematoxylin and eosin staining showed that inflammation was reduced and the stratum corneum had recovered in the 20 and 40 mL/kg LXD groups. LXD (20 and 40 mL/kg) significantly reduced IL-1β, IL-18 levels and the number of neutrophils in vaginal lavage and decreased TLR2, TLR4, MyD88, NF-κB, NLRP3, ASC, and caspase-1 expression. This study systematically demonstrated the therapeutic effect of LXD on protein expression and pathological conditions in VVC mice. The results showed that LXD could eliminate the invasion of vaginal hyphae in mice, reduce the recruitment of neutrophils, and reduce the expression of TLR/MyD88 pathway-related proteins and NLRP3 inflammasome. The above results clearly indicate that LXD may profoundly regulate NLRP3 inflammasome through the TLR/MyD88 pathway and play a therapeutic role in VVC. [Display omitted] •
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It has been used extensively to treat vulvovaginal candidiasis (VVC). However, despite its effectiveness, the mechanism of action remains unknown. To elucidate the mechanism by which LXD relieves VVC via the Toll-like receptor/MyD88 pathway and activation of the NLRP3 inflammasome. Female Kunming mice (n = 96) were randomly divided into six groups: control, VVC model, LXD (10/20/40 mL/kg), and positive drug fluconazole. Mice were vaginally administered Candida albicans (C. albicans) solution (20 μL; 1 × 108 colony-forming units/mL), suspended for 5 min, and observed daily for changes in their condition. Continuous dilution was used to determine the number of colony-forming units. Gram, periodic acid-Schiff, Papanicolaou, and hematoxylin and eosin staining were used to determine the extent of infection. Enzyme-linked immunosorbent assay(ELISA) was used to determine the levels of proinflammatory cytokines IL-1β and IL-18. TLR2, TLR4, MyD88, NF-κB, NLRP3, ASC, and caspase-1 protein expression were determined using western blotting. C. albicans infection destroyed the integrity of the vaginal mucosa, increased fungal burden and the influx of neutrophils into the vaginal cavity, and promoted the secretion of proinflammatory cytokines. C. albicans stimulated the expression of TLR2, TLR4, MyD88, NF-κB, NLRP3, ASC, and caspase-1 in vaginal tissue. Fungal burden, hyphal formation, and C. albicans adhesion were reduced in the 20 and 40 mL/kg LXD groups. Hematoxylin and eosin staining showed that inflammation was reduced and the stratum corneum had recovered in the 20 and 40 mL/kg LXD groups. LXD (20 and 40 mL/kg) significantly reduced IL-1β, IL-18 levels and the number of neutrophils in vaginal lavage and decreased TLR2, TLR4, MyD88, NF-κB, NLRP3, ASC, and caspase-1 expression. This study systematically demonstrated the therapeutic effect of LXD on protein expression and pathological conditions in VVC mice. The results showed that LXD could eliminate the invasion of vaginal hyphae in mice, reduce the recruitment of neutrophils, and reduce the expression of TLR/MyD88 pathway-related proteins and NLRP3 inflammasome. The above results clearly indicate that LXD may profoundly regulate NLRP3 inflammasome through the TLR/MyD88 pathway and play a therapeutic role in VVC. [Display omitted] •LDX exhibits significant efficacy against VVC.•LDX effectively reduces inflammatory damage to vaginal tissue, infiltration of neutrophils into the vagina, and the levels of proinflammatory cytokines in vaginal tissue.•LDX effectively lowers the expression level of NLRP3 inflammasome in vaginal tissue.•LDX downregulates the Toll-like receptor/MyD88 signaling pathway that governs NLRP3 inflammasome.</description><identifier>ISSN: 0378-8741</identifier><identifier>EISSN: 1872-7573</identifier><identifier>DOI: 10.1016/j.jep.2023.116869</identifier><identifier>PMID: 37390876</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Candida albicans ; Longdan Xiegan decoction ; NLRP3 inflammasome ; TLR/MyD88 pathway ; Vulvovaginal candidiasis</subject><ispartof>Journal of ethnopharmacology, 2024-01, Vol.318 (Pt A), p.116869-116869, Article 116869</ispartof><rights>2023 Elsevier B.V.</rights><rights>Copyright © 2023 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-a81acec9433230a5ea6ece37e88c6a0b62b6d0cc3ebfe6989d83877f6054f5b43</citedby><cites>FETCH-LOGICAL-c396t-a81acec9433230a5ea6ece37e88c6a0b62b6d0cc3ebfe6989d83877f6054f5b43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jep.2023.116869$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27926,27927,45997</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37390876$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Feng, Xin</creatorcontrib><creatorcontrib>Zhang, Hao</creatorcontrib><creatorcontrib>Hu, Kaifan</creatorcontrib><creatorcontrib>Shi, Gaoxiang</creatorcontrib><creatorcontrib>Wu, Daqiang</creatorcontrib><creatorcontrib>Shao, Jing</creatorcontrib><creatorcontrib>Wang, Tianming</creatorcontrib><creatorcontrib>Wang, Changzhong</creatorcontrib><title>Longdan Xiegan decoction ameliorates vulvovaginal candidiasis by inhibiting the NLRP3 inflammasome via the Toll-like receptor /MyD88 pathway</title><title>Journal of ethnopharmacology</title><addtitle>J Ethnopharmacol</addtitle><description>Longdan Xiegan decoction (LXD) is a standardized herbal prescription originally documented in the “Medical Formula Collection” by the eminent physician Wang Ang during the Qing dynasty. It has been used extensively to treat vulvovaginal candidiasis (VVC). However, despite its effectiveness, the mechanism of action remains unknown. To elucidate the mechanism by which LXD relieves VVC via the Toll-like receptor/MyD88 pathway and activation of the NLRP3 inflammasome. Female Kunming mice (n = 96) were randomly divided into six groups: control, VVC model, LXD (10/20/40 mL/kg), and positive drug fluconazole. Mice were vaginally administered Candida albicans (C. albicans) solution (20 μL; 1 × 108 colony-forming units/mL), suspended for 5 min, and observed daily for changes in their condition. Continuous dilution was used to determine the number of colony-forming units. Gram, periodic acid-Schiff, Papanicolaou, and hematoxylin and eosin staining were used to determine the extent of infection. Enzyme-linked immunosorbent assay(ELISA) was used to determine the levels of proinflammatory cytokines IL-1β and IL-18. TLR2, TLR4, MyD88, NF-κB, NLRP3, ASC, and caspase-1 protein expression were determined using western blotting. C. albicans infection destroyed the integrity of the vaginal mucosa, increased fungal burden and the influx of neutrophils into the vaginal cavity, and promoted the secretion of proinflammatory cytokines. C. albicans stimulated the expression of TLR2, TLR4, MyD88, NF-κB, NLRP3, ASC, and caspase-1 in vaginal tissue. Fungal burden, hyphal formation, and C. albicans adhesion were reduced in the 20 and 40 mL/kg LXD groups. Hematoxylin and eosin staining showed that inflammation was reduced and the stratum corneum had recovered in the 20 and 40 mL/kg LXD groups. LXD (20 and 40 mL/kg) significantly reduced IL-1β, IL-18 levels and the number of neutrophils in vaginal lavage and decreased TLR2, TLR4, MyD88, NF-κB, NLRP3, ASC, and caspase-1 expression. This study systematically demonstrated the therapeutic effect of LXD on protein expression and pathological conditions in VVC mice. The results showed that LXD could eliminate the invasion of vaginal hyphae in mice, reduce the recruitment of neutrophils, and reduce the expression of TLR/MyD88 pathway-related proteins and NLRP3 inflammasome. The above results clearly indicate that LXD may profoundly regulate NLRP3 inflammasome through the TLR/MyD88 pathway and play a therapeutic role in VVC. [Display omitted] •LDX exhibits significant efficacy against VVC.•LDX effectively reduces inflammatory damage to vaginal tissue, infiltration of neutrophils into the vagina, and the levels of proinflammatory cytokines in vaginal tissue.•LDX effectively lowers the expression level of NLRP3 inflammasome in vaginal tissue.•LDX downregulates the Toll-like receptor/MyD88 signaling pathway that governs NLRP3 inflammasome.</description><subject>Candida albicans</subject><subject>Longdan Xiegan decoction</subject><subject>NLRP3 inflammasome</subject><subject>TLR/MyD88 pathway</subject><subject>Vulvovaginal candidiasis</subject><issn>0378-8741</issn><issn>1872-7573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kUFv1DAQhS0EokvhB3BBPnLJ1o4T2xEnVFpAWihCReJmTZzJ7ixOHOJs0P6H_mhStnDkNNLMe5807zH2Uoq1FFJf7Nd7HNa5yNVaSm119YitpDV5ZkqjHrOVUMZm1hTyjD1LaS-EMLIQT9mZMqoS1ugVu9vEfttAz78TbpfRoI9-othz6DBQHGHCxOdDmOMMW-ohcA99Qw1BosTrI6d-RzVN1G_5tEP-efP1i1qWbYCugxQ75DPBn9NtDCEL9AP5iB6HKY784tPxnbV8gGn3C47P2ZMWQsIXD_Ocfbu-ur38kG1u3n-8fLvJvKr0lIGV4NFXhVK5ElAi6IWnDFrrNYha57VuhPcK6xZ1ZavGKmtMq0VZtGVdqHP2-sQdxvjzgGlyHSWPIUCP8ZBcblVeGptX5SKVJ6kfY0ojtm4YqYPx6KRw9yW4vVtKcPcluFMJi-fVA_5Qd9j8c_xNfRG8OQlweXImHF3yhL3HhpZkJtdE-g_-N_A5mfY</recordid><startdate>20240110</startdate><enddate>20240110</enddate><creator>Feng, Xin</creator><creator>Zhang, Hao</creator><creator>Hu, Kaifan</creator><creator>Shi, Gaoxiang</creator><creator>Wu, Daqiang</creator><creator>Shao, Jing</creator><creator>Wang, Tianming</creator><creator>Wang, Changzhong</creator><general>Elsevier B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20240110</creationdate><title>Longdan Xiegan decoction ameliorates vulvovaginal candidiasis by inhibiting the NLRP3 inflammasome via the Toll-like receptor /MyD88 pathway</title><author>Feng, Xin ; Zhang, Hao ; Hu, Kaifan ; Shi, Gaoxiang ; Wu, Daqiang ; Shao, Jing ; Wang, Tianming ; Wang, Changzhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-a81acec9433230a5ea6ece37e88c6a0b62b6d0cc3ebfe6989d83877f6054f5b43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Candida albicans</topic><topic>Longdan Xiegan decoction</topic><topic>NLRP3 inflammasome</topic><topic>TLR/MyD88 pathway</topic><topic>Vulvovaginal candidiasis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Feng, Xin</creatorcontrib><creatorcontrib>Zhang, Hao</creatorcontrib><creatorcontrib>Hu, Kaifan</creatorcontrib><creatorcontrib>Shi, Gaoxiang</creatorcontrib><creatorcontrib>Wu, Daqiang</creatorcontrib><creatorcontrib>Shao, Jing</creatorcontrib><creatorcontrib>Wang, Tianming</creatorcontrib><creatorcontrib>Wang, Changzhong</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of ethnopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Feng, Xin</au><au>Zhang, Hao</au><au>Hu, Kaifan</au><au>Shi, Gaoxiang</au><au>Wu, Daqiang</au><au>Shao, Jing</au><au>Wang, Tianming</au><au>Wang, Changzhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Longdan Xiegan decoction ameliorates vulvovaginal candidiasis by inhibiting the NLRP3 inflammasome via the Toll-like receptor /MyD88 pathway</atitle><jtitle>Journal of ethnopharmacology</jtitle><addtitle>J Ethnopharmacol</addtitle><date>2024-01-10</date><risdate>2024</risdate><volume>318</volume><issue>Pt A</issue><spage>116869</spage><epage>116869</epage><pages>116869-116869</pages><artnum>116869</artnum><issn>0378-8741</issn><eissn>1872-7573</eissn><abstract>Longdan Xiegan decoction (LXD) is a standardized herbal prescription originally documented in the “Medical Formula Collection” by the eminent physician Wang Ang during the Qing dynasty. It has been used extensively to treat vulvovaginal candidiasis (VVC). However, despite its effectiveness, the mechanism of action remains unknown. To elucidate the mechanism by which LXD relieves VVC via the Toll-like receptor/MyD88 pathway and activation of the NLRP3 inflammasome. Female Kunming mice (n = 96) were randomly divided into six groups: control, VVC model, LXD (10/20/40 mL/kg), and positive drug fluconazole. Mice were vaginally administered Candida albicans (C. albicans) solution (20 μL; 1 × 108 colony-forming units/mL), suspended for 5 min, and observed daily for changes in their condition. Continuous dilution was used to determine the number of colony-forming units. Gram, periodic acid-Schiff, Papanicolaou, and hematoxylin and eosin staining were used to determine the extent of infection. Enzyme-linked immunosorbent assay(ELISA) was used to determine the levels of proinflammatory cytokines IL-1β and IL-18. TLR2, TLR4, MyD88, NF-κB, NLRP3, ASC, and caspase-1 protein expression were determined using western blotting. C. albicans infection destroyed the integrity of the vaginal mucosa, increased fungal burden and the influx of neutrophils into the vaginal cavity, and promoted the secretion of proinflammatory cytokines. C. albicans stimulated the expression of TLR2, TLR4, MyD88, NF-κB, NLRP3, ASC, and caspase-1 in vaginal tissue. Fungal burden, hyphal formation, and C. albicans adhesion were reduced in the 20 and 40 mL/kg LXD groups. Hematoxylin and eosin staining showed that inflammation was reduced and the stratum corneum had recovered in the 20 and 40 mL/kg LXD groups. LXD (20 and 40 mL/kg) significantly reduced IL-1β, IL-18 levels and the number of neutrophils in vaginal lavage and decreased TLR2, TLR4, MyD88, NF-κB, NLRP3, ASC, and caspase-1 expression. This study systematically demonstrated the therapeutic effect of LXD on protein expression and pathological conditions in VVC mice. The results showed that LXD could eliminate the invasion of vaginal hyphae in mice, reduce the recruitment of neutrophils, and reduce the expression of TLR/MyD88 pathway-related proteins and NLRP3 inflammasome. The above results clearly indicate that LXD may profoundly regulate NLRP3 inflammasome through the TLR/MyD88 pathway and play a therapeutic role in VVC. [Display omitted] •LDX exhibits significant efficacy against VVC.•LDX effectively reduces inflammatory damage to vaginal tissue, infiltration of neutrophils into the vagina, and the levels of proinflammatory cytokines in vaginal tissue.•LDX effectively lowers the expression level of NLRP3 inflammasome in vaginal tissue.•LDX downregulates the Toll-like receptor/MyD88 signaling pathway that governs NLRP3 inflammasome.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>37390876</pmid><doi>10.1016/j.jep.2023.116869</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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subjects Candida albicans
Longdan Xiegan decoction
NLRP3 inflammasome
TLR/MyD88 pathway
Vulvovaginal candidiasis
title Longdan Xiegan decoction ameliorates vulvovaginal candidiasis by inhibiting the NLRP3 inflammasome via the Toll-like receptor /MyD88 pathway
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