RapamycinFungusV1, Main, Exploration, bibRecord, 000863

Eburicoic acid from Laetiporus sulphureus (Bull.:Fr.) Murrill attenuates inflammatory responses through inhibiting LPS-induced activation of PI3K/Akt/mTOR/NF-κB pathways in RAW264.7 cells.

Identifieur interne : 000863 ( Main/Exploration ); précédent : 000862; suivant : 000864

Eburicoic acid from Laetiporus sulphureus (Bull.:Fr.) Murrill attenuates inflammatory responses through inhibiting LPS-induced activation of PI3K/Akt/mTOR/NF-κB pathways in RAW264.7 cells.

Auteurs : Junzhi Wang [République populaire de Chine] ; Pan Zhang [République populaire de Chine] ; Haibo He [République populaire de Chine] ; Xinxin Se [République populaire de Chine] ; Wenjun Sun [République populaire de Chine] ; Beiyan Chen [République populaire de Chine] ; Lin Zhang [République populaire de Chine] ; Ximing Yan [République populaire de Chine] ; Kun Zou [République populaire de Chine]

Source :

Naunyn-Schmiedeberg's archives of pharmacology [ 1432-1912 ] ; 2017.

RBID : pubmed:28577049

Descripteurs français

KwdFr :
- Animaux (MeSH), Anti-inflammatoires (pharmacologie), Cellules RAW 264.7 (MeSH), Cyclooxygenase 2 (génétique), Cytokines (génétique), Cytokines (métabolisme), Dinoprostone (métabolisme), Facteur de transcription RelA (métabolisme), Lanostérol (analogues et dérivés), Lanostérol (pharmacologie), Lipopolysaccharides (MeSH), Monoxyde d'azote (métabolisme), Nitric oxide synthase type II (génétique), Phosphatidylinositol 3-kinase (métabolisme), Polyporales (MeSH), Protéines proto-oncogènes c-akt (métabolisme), Souris (MeSH), Survie cellulaire (effets des médicaments et des substances chimiques), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (MeSH).
MESH :
- analogues et dérivés : Lanostérol.
- effets des médicaments et des substances chimiques : Survie cellulaire.
- génétique : Cyclooxygenase 2, Cytokines, Nitric oxide synthase type II.
- métabolisme : Cytokines, Dinoprostone, Facteur de transcription RelA, Monoxyde d'azote, Phosphatidylinositol 3-kinase, Protéines proto-oncogènes c-akt, Sérine-thréonine kinases TOR.
- pharmacologie : Anti-inflammatoires, Lanostérol.
- Animaux, Cellules RAW 264.7, Lipopolysaccharides, Polyporales, Souris, Transduction du signal.

English descriptors

KwdEn :
- Animals (MeSH), Anti-Inflammatory Agents (pharmacology), Cell Survival (drug effects), Cyclooxygenase 2 (genetics), Cytokines (genetics), Cytokines (metabolism), Dinoprostone (metabolism), Lanosterol (analogs & derivatives), Lanosterol (pharmacology), Lipopolysaccharides (MeSH), Mice (MeSH), Nitric Oxide (metabolism), Nitric Oxide Synthase Type II (genetics), Phosphatidylinositol 3-Kinase (metabolism), Polyporales (MeSH), Proto-Oncogene Proteins c-akt (metabolism), RAW 264.7 Cells (MeSH), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (metabolism), Transcription Factor RelA (metabolism).
MESH :
- chemical , analogs & derivatives : Lanosterol.
- chemical , genetics : Cyclooxygenase 2, Cytokines, Nitric Oxide Synthase Type II.
- chemical , metabolism : Cytokines, Dinoprostone, Nitric Oxide, Phosphatidylinositol 3-Kinase, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases, Transcription Factor RelA.
- chemical , pharmacology : Anti-Inflammatory Agents, Lanosterol.
- drug effects : Cell Survival.
- Animals, Lipopolysaccharides, Mice, Polyporales, RAW 264.7 Cells, Signal Transduction.

Abstract

Excessive activation of macrophages has been implicated in various types of inflammatory injury. Suppression of macrophage activation would have therapeutic benefits, leading to the alleviation of the progression of inflammatory diseases. Eburicoic acid (EA) is one of main bioactive components isolated from Laetiporus sulphureus (Bull.:Fr.) Murrill. In our previous study, we found that EA possessed anti-inflammatory activities. However, the cellular and molecular mechanisms underlying its anti-inflammatory activities remain to be poorly understood. The present study aimed to further evaluate its effect on lipopolysaccharide (LPS)-induced inflammatory responses in RAW264.7 macrophage cells. We investigated the anti-inflammatory effect by modulating LPS-induced activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR)/nuclear transcription factor-κB (NF-κB) pathway in RAW264.7 cells. The results showed that EA caused no obvious cytotoxicity, and its suitable concentrations on RAW264.7 cells were in the range from 0.02 to 0.08 μM. EA significantly inhibited the releases of inflammatory mediators, nitrite oxide (NO) and prostaglandin E2 (PGE₂); suppressed mRNA and protein expression levels of inducible nitrite oxide synthase (iNOS) and cyclooxygenase-2 COX-2 and pro-inflammatory cytokine TNF-α, IL-6, and IL-1β; and reduced levels of phosphorylated PI3K, Akt, mTOR, and NF-κBp65 in LPS-induced RAW264.7 cells in dose- and time-dependent manners. These aforementioned results indicated that EA executed anti-inflammatory effect on LPS-induced RAW264.7 cells, and this effect might be achieved via suppressing the PI3K/Akt/mTOR/NF-κB signaling pathway and inhibiting the LPS-induced productions of inflammatory mediators and pro-inflammatory cytokines.

DOI: 10.1007/s00210-017-1382-3
PubMed: 28577049

Affiliations:

République populaire de Chine

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000800
to stream Main, to step Curation: 000800

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Anti-Inflammatory Agents (pharmacology)</term>
<term>Cell Survival (drug effects)</term>
<term>Cyclooxygenase 2 (genetics)</term>
<term>Cytokines (genetics)</term>
<term>Cytokines (metabolism)</term>
<term>Dinoprostone (metabolism)</term>
<term>Lanosterol (analogs & derivatives)</term>
<term>Lanosterol (pharmacology)</term>
<term>Lipopolysaccharides (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Nitric Oxide (metabolism)</term>
<term>Nitric Oxide Synthase Type II (genetics)</term>
<term>Phosphatidylinositol 3-Kinase (metabolism)</term>
<term>Polyporales (MeSH)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>RAW 264.7 Cells (MeSH)</term>
<term>Signal Transduction (MeSH)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Transcription Factor RelA (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Anti-inflammatoires (pharmacologie)</term>
<term>Cellules RAW 264.7 (MeSH)</term>
<term>Cyclooxygenase 2 (génétique)</term>
<term>Cytokines (génétique)</term>
<term>Cytokines (métabolisme)</term>
<term>Dinoprostone (métabolisme)</term>
<term>Facteur de transcription RelA (métabolisme)</term>
<term>Lanostérol (analogues et dérivés)</term>
<term>Lanostérol (pharmacologie)</term>
<term>Lipopolysaccharides (MeSH)</term>
<term>Monoxyde d'azote (métabolisme)</term>
<term>Nitric oxide synthase type II (génétique)</term>
<term>Phosphatidylinositol 3-kinase (métabolisme)</term>
<term>Polyporales (MeSH)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Survie cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Transduction du signal (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Lanosterol</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cyclooxygenase 2</term>
<term>Cytokines</term>
<term>Nitric Oxide Synthase Type II</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term>
<term>Dinoprostone</term>
<term>Nitric Oxide</term>
<term>Phosphatidylinositol 3-Kinase</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Transcription Factor RelA</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents</term>
<term>Lanosterol</term>
</keywords>
<keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Lanostérol</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Survival</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Survie cellulaire</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Cyclooxygenase 2</term>
<term>Cytokines</term>
<term>Nitric oxide synthase type II</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term>
<term>Dinoprostone</term>
<term>Facteur de transcription RelA</term>
<term>Monoxyde d'azote</term>
<term>Phosphatidylinositol 3-kinase</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Sérine-thréonine kinases TOR</term>
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<term>Lanostérol</term>
</keywords>
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<term>Lipopolysaccharides</term>
<term>Mice</term>
<term>Polyporales</term>
<term>RAW 264.7 Cells</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules RAW 264.7</term>
<term>Lipopolysaccharides</term>
<term>Polyporales</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">Excessive activation of macrophages has been implicated in various types of inflammatory injury. Suppression of macrophage activation would have therapeutic benefits, leading to the alleviation of the progression of inflammatory diseases. Eburicoic acid (EA) is one of main bioactive components isolated from Laetiporus sulphureus (Bull.:Fr.) Murrill. In our previous study, we found that EA possessed anti-inflammatory activities. However, the cellular and molecular mechanisms underlying its anti-inflammatory activities remain to be poorly understood. The present study aimed to further evaluate its effect on lipopolysaccharide (LPS)-induced inflammatory responses in RAW264.7 macrophage cells. We investigated the anti-inflammatory effect by modulating LPS-induced activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR)/nuclear transcription factor-κB (NF-κB) pathway in RAW264.7 cells. The results showed that EA caused no obvious cytotoxicity, and its suitable concentrations on RAW264.7 cells were in the range from 0.02 to 0.08 μM. EA significantly inhibited the releases of inflammatory mediators, nitrite oxide (NO) and prostaglandin E2 (PGE<sub>2</sub>
); suppressed mRNA and protein expression levels of inducible nitrite oxide synthase (iNOS) and cyclooxygenase-2 COX-2 and pro-inflammatory cytokine TNF-α, IL-6, and IL-1β; and reduced levels of phosphorylated PI3K, Akt, mTOR, and NF-κBp65 in LPS-induced RAW264.7 cells in dose- and time-dependent manners. These aforementioned results indicated that EA executed anti-inflammatory effect on LPS-induced RAW264.7 cells, and this effect might be achieved via suppressing the PI3K/Akt/mTOR/NF-κB signaling pathway and inhibiting the LPS-induced productions of inflammatory mediators and pro-inflammatory cytokines.</div>
</front>
</TEI>
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<DateCompleted><Year>2018</Year>
<Month>05</Month>
<Day>09</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1432-1912</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>390</Volume>
<Issue>8</Issue>
<PubDate><Year>2017</Year>
<Month>Aug</Month>
</PubDate>
</JournalIssue>
<Title>Naunyn-Schmiedeberg's archives of pharmacology</Title>
<ISOAbbreviation>Naunyn Schmiedebergs Arch Pharmacol</ISOAbbreviation>
</Journal>
<ArticleTitle>Eburicoic acid from Laetiporus sulphureus (Bull.:Fr.) Murrill attenuates inflammatory responses through inhibiting LPS-induced activation of PI3K/Akt/mTOR/NF-κB pathways in RAW264.7 cells.</ArticleTitle>
<Pagination><MedlinePgn>845-856</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1007/s00210-017-1382-3</ELocationID>
<Abstract><AbstractText>Excessive activation of macrophages has been implicated in various types of inflammatory injury. Suppression of macrophage activation would have therapeutic benefits, leading to the alleviation of the progression of inflammatory diseases. Eburicoic acid (EA) is one of main bioactive components isolated from Laetiporus sulphureus (Bull.:Fr.) Murrill. In our previous study, we found that EA possessed anti-inflammatory activities. However, the cellular and molecular mechanisms underlying its anti-inflammatory activities remain to be poorly understood. The present study aimed to further evaluate its effect on lipopolysaccharide (LPS)-induced inflammatory responses in RAW264.7 macrophage cells. We investigated the anti-inflammatory effect by modulating LPS-induced activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR)/nuclear transcription factor-κB (NF-κB) pathway in RAW264.7 cells. The results showed that EA caused no obvious cytotoxicity, and its suitable concentrations on RAW264.7 cells were in the range from 0.02 to 0.08 μM. EA significantly inhibited the releases of inflammatory mediators, nitrite oxide (NO) and prostaglandin E2 (PGE<sub>2</sub>
); suppressed mRNA and protein expression levels of inducible nitrite oxide synthase (iNOS) and cyclooxygenase-2 COX-2 and pro-inflammatory cytokine TNF-α, IL-6, and IL-1β; and reduced levels of phosphorylated PI3K, Akt, mTOR, and NF-κBp65 in LPS-induced RAW264.7 cells in dose- and time-dependent manners. These aforementioned results indicated that EA executed anti-inflammatory effect on LPS-induced RAW264.7 cells, and this effect might be achieved via suppressing the PI3K/Akt/mTOR/NF-κB signaling pathway and inhibiting the LPS-induced productions of inflammatory mediators and pro-inflammatory cytokines.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Junzhi</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Hubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Hubei Research Institute of Tujia Medicine, China Three Gorges University, Yichang, Hubei, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Pan</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Hubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>He</LastName>
<ForeName>Haibo</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Hubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China. hehaibo252219@163.com.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Hubei Research Institute of Tujia Medicine, China Three Gorges University, Yichang, Hubei, China. hehaibo252219@163.com.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Se</LastName>
<ForeName>Xinxin</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Hubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Wenjun</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Hubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Beiyan</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Hubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Lin</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Hubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yan</LastName>
<ForeName>Ximing</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Hubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zou</LastName>
<ForeName>Kun</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Hubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Hubei Research Institute of Tujia Medicine, China Three Gorges University, Yichang, Hubei, China.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
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</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>06</Month>
<Day>02</Day>
</ArticleDate>
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<MedlineTA>Naunyn Schmiedebergs Arch Pharmacol</MedlineTA>
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<MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D000067996" MajorTopicYN="N">RAW 264.7 Cells</DescriptorName>
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<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
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<MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName>
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<Keyword MajorTopicYN="N">Inflammatory mediators</Keyword>
<Keyword MajorTopicYN="N">PI3K/Akt/mTOR/NF-κB signaling pathway</Keyword>
<Keyword MajorTopicYN="N">Pro-inflammatory cytokines</Keyword>
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<name sortKey="Wang, Junzhi" sort="Wang, Junzhi" uniqKey="Wang J" first="Junzhi" last="Wang">Junzhi Wang</name>
<name sortKey="Yan, Ximing" sort="Yan, Ximing" uniqKey="Yan X" first="Ximing" last="Yan">Ximing Yan</name>
<name sortKey="Zhang, Lin" sort="Zhang, Lin" uniqKey="Zhang L" first="Lin" last="Zhang">Lin Zhang</name>
<name sortKey="Zhang, Pan" sort="Zhang, Pan" uniqKey="Zhang P" first="Pan" last="Zhang">Pan Zhang</name>
<name sortKey="Zou, Kun" sort="Zou, Kun" uniqKey="Zou K" first="Kun" last="Zou">Kun Zou</name>
<name sortKey="Zou, Kun" sort="Zou, Kun" uniqKey="Zou K" first="Kun" last="Zou">Kun Zou</name>
</country>
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   |clé=     pubmed:28577049
   |texte=   Eburicoic acid from Laetiporus sulphureus (Bull.:Fr.) Murrill attenuates inflammatory responses through inhibiting LPS-induced activation of PI3K/Akt/mTOR/NF-κB pathways in RAW264.7 cells.
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	Serveur d'exploration sur la rapamycine et les champignons
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Serveur d'exploration sur la rapamycine et les champignons

Eburicoic acid from Laetiporus sulphureus (Bull.:Fr.) Murrill attenuates inflammatory responses through inhibiting LPS-induced activation of PI3K/Akt/mTOR/NF-κB pathways in RAW264.7 cells.

Eburicoic acid from Laetiporus sulphureus (Bull.:Fr.) Murrill attenuates inflammatory responses through inhibiting LPS-induced activation of PI3K/Akt/mTOR/NF-κB pathways in RAW264.7 cells.

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