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 : 000800 ( Main/Corpus ); précédent : 000799; suivant : 000801Eburicoic 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 ; Pan Zhang ; Haibo He ; Xinxin Se ; Wenjun Sun ; Beiyan Chen ; Lin Zhang ; Ximing Yan ; Kun ZouSource :
- Naunyn-Schmiedeberg's archives of pharmacology [ 1432-1912 ] ; 2017.
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
Links to Exploration step
pubmed:28577049Le document en format XML
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<term>Cyclooxygenase 2 (genetics)</term>
<term>Cytokines (genetics)</term>
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<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="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Lanosterol</term>
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<term>Nitric Oxide Synthase Type II</term>
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<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>
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<term>Lipopolysaccharides</term>
<term>Mice</term>
<term>Polyporales</term>
<term>RAW 264.7 Cells</term>
<term>Signal Transduction</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>
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<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>
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<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>
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