Luteoloside Protects the Uterus from Staphylococcus aureus-Induced Inflammation, Apoptosis, and Injury

Luteoloside is a flavonoid extracted from several natural herbs that exhibits anti-microbial and anti-inflammation properties. Our study mainly identified the anti-inflammatory mechanism of action of luteoloside in Staphylococcus aureus -induced endometritis. Histopathological observations and myelo...

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Veröffentlicht in:Inflammation 2018-10, Vol.41 (5), p.1702-1716
Hauptverfasser: Wang, Xiaoyan, Yuan, Ting, Yin, Nannan, Ma, Xiaofei, Zhang, Zhenbiao, Zhu, Zhe, Shaukat, Aftab, Deng, Ganzhen
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container_end_page 1716
container_issue 5
container_start_page 1702
container_title Inflammation
container_volume 41
creator Wang, Xiaoyan
Yuan, Ting
Yin, Nannan
Ma, Xiaofei
Zhang, Zhenbiao
Zhu, Zhe
Shaukat, Aftab
Deng, Ganzhen
description Luteoloside is a flavonoid extracted from several natural herbs that exhibits anti-microbial and anti-inflammation properties. Our study mainly identified the anti-inflammatory mechanism of action of luteoloside in Staphylococcus aureus -induced endometritis. Histopathological observations and myeloperoxidase (MPO) activity showed that luteoloside could protect the uterus from S. aureus -induced damage and ameliorate the infiltration of inflammatory cells. Quantitative PCR (qPCR) and ELISA analysis also revealed that luteoloside could decrease the expression of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 and increase the expression of the anti-inflammatory cytokine IL-10 both in vivo and in vitro . However, western blot analysis revealed that luteoloside inhibited the expression of TLR2 and IL-8 and inhibited the phosphorylation of IκBα and NF-κB p65. Moreover, luteoloside inhibited the apoptosis of endometrial epithelial cells (EECs), suppressed the phosphorylation of p53, and decreased the expression of caspase-3 induced by S. aureus . Furthermore, this study showed that luteoloside inhibited the expression of Bax but increased the expression of Bcl-2. These results indicate that luteoloside has anti-inflammatory properties by inhibiting the TLR2 and NF-κB signaling pathways and plays an anti-apoptotic role in S. aureus -induced endometritis, which may be valuable for the clinical treatment of S. aureus -induced inflammation.
doi_str_mv 10.1007/s10753-018-0814-7
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Our study mainly identified the anti-inflammatory mechanism of action of luteoloside in Staphylococcus aureus -induced endometritis. Histopathological observations and myeloperoxidase (MPO) activity showed that luteoloside could protect the uterus from S. aureus -induced damage and ameliorate the infiltration of inflammatory cells. Quantitative PCR (qPCR) and ELISA analysis also revealed that luteoloside could decrease the expression of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 and increase the expression of the anti-inflammatory cytokine IL-10 both in vivo and in vitro . However, western blot analysis revealed that luteoloside inhibited the expression of TLR2 and IL-8 and inhibited the phosphorylation of IκBα and NF-κB p65. Moreover, luteoloside inhibited the apoptosis of endometrial epithelial cells (EECs), suppressed the phosphorylation of p53, and decreased the expression of caspase-3 induced by S. aureus . 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Our study mainly identified the anti-inflammatory mechanism of action of luteoloside in Staphylococcus aureus -induced endometritis. Histopathological observations and myeloperoxidase (MPO) activity showed that luteoloside could protect the uterus from S. aureus -induced damage and ameliorate the infiltration of inflammatory cells. Quantitative PCR (qPCR) and ELISA analysis also revealed that luteoloside could decrease the expression of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 and increase the expression of the anti-inflammatory cytokine IL-10 both in vivo and in vitro . However, western blot analysis revealed that luteoloside inhibited the expression of TLR2 and IL-8 and inhibited the phosphorylation of IκBα and NF-κB p65. Moreover, luteoloside inhibited the apoptosis of endometrial epithelial cells (EECs), suppressed the phosphorylation of p53, and decreased the expression of caspase-3 induced by S. aureus . Furthermore, this study showed that luteoloside inhibited the expression of Bax but increased the expression of Bcl-2. These results indicate that luteoloside has anti-inflammatory properties by inhibiting the TLR2 and NF-κB signaling pathways and plays an anti-apoptotic role in S. aureus -induced endometritis, which may be valuable for the clinical treatment of S. aureus -induced inflammation.</description><subject>Animals</subject><subject>Anti-inflammatory agents</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Bcl-2 protein</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cytokines - drug effects</subject><subject>Cytokines - metabolism</subject><subject>Endometritis</subject><subject>Endometritis - drug therapy</subject><subject>Endometritis - microbiology</subject><subject>Endometrium</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Epithelial cells</subject><subject>Female</subject><subject>Glucosides - pharmacology</subject><subject>Glucosides - therapeutic use</subject><subject>Humans</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - microbiology</subject><subject>Interleukin 10</subject><subject>Interleukin 6</subject><subject>Interleukin 8</subject><subject>Internal Medicine</subject><subject>Luteolin - pharmacology</subject><subject>Luteolin - therapeutic use</subject><subject>NF-kappa B - drug effects</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Original Article</subject><subject>p53 Protein</subject><subject>Pathology</subject><subject>Peroxidase</subject><subject>Pharmacology/Toxicology</subject><subject>Phosphorylation</subject><subject>Protective Agents - therapeutic use</subject><subject>Rheumatology</subject><subject>Staphylococcus aureus</subject><subject>Staphylococcus aureus - pathogenicity</subject><subject>TLR2 protein</subject><subject>Toll-Like Receptor 2 - drug effects</subject><subject>Toll-Like Receptor 2 - metabolism</subject><subject>Toll-like receptors</subject><subject>Tumor necrosis factor-α</subject><subject>Uterus</subject><subject>Uterus - injuries</subject><subject>Uterus - microbiology</subject><subject>Uterus - pathology</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kU1r3DAQhkVpaTYfP6CXYuilh6gdWdbXMYS0WVhIoelZyJLc7GJbrj4O--8js2kLhZ4GZp5552VehN4R-EQAxOdEQDCKgUgMknRYvEIbwgTFLRP8NdoA5YCpUuIMnad0AACpJH2LzlqlpOgk2aBhV7IPY0h755tvMWRvc2ryk29-ZB9LaoYYpuZ7NsvTcQw2WFt7pkRfEt7Orljvmu08jGaaTN6H-bq5WcKSq166bsy8Dg8lHi_Rm8GMyV-91Av0-OXu8fYe7x6-bm9vdthS0WasDDFCCt87xVs6MK6YtNWnNEPfedqxfnA9aUECG5Rj0DlQgntGDJWKO3qBPp5klxh-FZ-ynvbJ-nE0sw8l6Ra4kJIJRSv64R_0EEqcq7mV4lJw4CtFTpSNIaXoB73E_WTiURPQawb6lIGuGeg1Ay3qzvsX5dJP3v3Z-P30CrQnINXR_NPHv6f_r_oMRbSR3w</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Wang, Xiaoyan</creator><creator>Yuan, Ting</creator><creator>Yin, Nannan</creator><creator>Ma, Xiaofei</creator><creator>Zhang, Zhenbiao</creator><creator>Zhu, Zhe</creator><creator>Shaukat, Aftab</creator><creator>Deng, Ganzhen</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8190-0040</orcidid></search><sort><creationdate>20181001</creationdate><title>Luteoloside Protects the Uterus from Staphylococcus aureus-Induced Inflammation, Apoptosis, and Injury</title><author>Wang, Xiaoyan ; 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Our study mainly identified the anti-inflammatory mechanism of action of luteoloside in Staphylococcus aureus -induced endometritis. Histopathological observations and myeloperoxidase (MPO) activity showed that luteoloside could protect the uterus from S. aureus -induced damage and ameliorate the infiltration of inflammatory cells. Quantitative PCR (qPCR) and ELISA analysis also revealed that luteoloside could decrease the expression of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 and increase the expression of the anti-inflammatory cytokine IL-10 both in vivo and in vitro . However, western blot analysis revealed that luteoloside inhibited the expression of TLR2 and IL-8 and inhibited the phosphorylation of IκBα and NF-κB p65. Moreover, luteoloside inhibited the apoptosis of endometrial epithelial cells (EECs), suppressed the phosphorylation of p53, and decreased the expression of caspase-3 induced by S. aureus . Furthermore, this study showed that luteoloside inhibited the expression of Bax but increased the expression of Bcl-2. These results indicate that luteoloside has anti-inflammatory properties by inhibiting the TLR2 and NF-κB signaling pathways and plays an anti-apoptotic role in S. aureus -induced endometritis, which may be valuable for the clinical treatment of S. aureus -induced inflammation.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>29987481</pmid><doi>10.1007/s10753-018-0814-7</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-8190-0040</orcidid></addata></record>
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subjects Animals
Anti-inflammatory agents
Apoptosis
Apoptosis - drug effects
Bcl-2 protein
Biomedical and Life Sciences
Biomedicine
Caspase
Caspase-3
Cytokines - drug effects
Cytokines - metabolism
Endometritis
Endometritis - drug therapy
Endometritis - microbiology
Endometrium
Enzyme-linked immunosorbent assay
Epithelial cells
Female
Glucosides - pharmacology
Glucosides - therapeutic use
Humans
Immunology
Inflammation
Inflammation - drug therapy
Inflammation - microbiology
Interleukin 10
Interleukin 6
Interleukin 8
Internal Medicine
Luteolin - pharmacology
Luteolin - therapeutic use
NF-kappa B - drug effects
NF-kappa B - metabolism
NF-κB protein
Original Article
p53 Protein
Pathology
Peroxidase
Pharmacology/Toxicology
Phosphorylation
Protective Agents - therapeutic use
Rheumatology
Staphylococcus aureus
Staphylococcus aureus - pathogenicity
TLR2 protein
Toll-Like Receptor 2 - drug effects
Toll-Like Receptor 2 - metabolism
Toll-like receptors
Tumor necrosis factor-α
Uterus
Uterus - injuries
Uterus - microbiology
Uterus - pathology
title Luteoloside Protects the Uterus from Staphylococcus aureus-Induced Inflammation, Apoptosis, and Injury
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