PoplarV1, Main, Exploration, bibRecord, 001032

Bioactive components and mechanisms of Chinese poplar propolis alleviates oxidized low-density lipoprotein-induced endothelial cells injury.

Identifieur interne : 001032 ( Main/Exploration ); précédent : 001031; suivant : 001033

Bioactive components and mechanisms of Chinese poplar propolis alleviates oxidized low-density lipoprotein-induced endothelial cells injury.

Auteurs : Huasong Chang [République populaire de Chine] ; Wenwen Yuan [République populaire de Chine] ; Haizhu Wu [République populaire de Chine] ; Xusheng Yin [République populaire de Chine] ; Hongzhuan Xuan [République populaire de Chine]

Source :

BMC complementary and alternative medicine [ 1472-6882 ] ; 2018.

RBID : pubmed:29724195

Descripteurs français

KwdFr :
- Apoptose (effets des médicaments et des substances chimiques), Autophagie (effets des médicaments et des substances chimiques), Cellules endothéliales de la veine ombilicale humaine (effets des médicaments et des substances chimiques), Chromatographie en phase liquide à haute performance (MeSH), Humains (MeSH), Lignée cellulaire (MeSH), Lipoprotéines LDL (effets indésirables), Populus (composition chimique), Propolis (pharmacologie), Protéines proto-oncogènes c-akt (métabolisme), Stress oxydatif (effets des médicaments et des substances chimiques), Survie cellulaire (effets des médicaments et des substances chimiques), p38 Mitogen-Activated Protein Kinases (métabolisme).
MESH :
- composition chimique : Populus.
- effets des médicaments et des substances chimiques : Apoptose, Autophagie, Cellules endothéliales de la veine ombilicale humaine, Stress oxydatif, Survie cellulaire.
- effets indésirables : Lipoprotéines LDL.
- métabolisme : Protéines proto-oncogènes c-akt, p38 Mitogen-Activated Protein Kinases.
- pharmacologie : Propolis.
- Chromatographie en phase liquide à haute performance, Humains, Lignée cellulaire.

English descriptors

KwdEn :
- Apoptosis (drug effects), Autophagy (drug effects), Cell Line (MeSH), Cell Survival (drug effects), Chromatography, High Pressure Liquid (MeSH), Human Umbilical Vein Endothelial Cells (drug effects), Humans (MeSH), Lipoproteins, LDL (adverse effects), Oxidative Stress (drug effects), Populus (chemistry), Propolis (pharmacology), Proto-Oncogene Proteins c-akt (metabolism), p38 Mitogen-Activated Protein Kinases (metabolism).
MESH :
- chemical , adverse effects : Lipoproteins, LDL.
- chemistry : Populus.
- drug effects : Apoptosis, Autophagy, Cell Survival, Human Umbilical Vein Endothelial Cells, Oxidative Stress.
- chemical , metabolism : Proto-Oncogene Proteins c-akt, p38 Mitogen-Activated Protein Kinases.
- chemical , pharmacology : Propolis.
- Cell Line, Chromatography, High Pressure Liquid, Humans.

Abstract

BACKGROUND

Propolis, a polyphenol-rich natural product, has been used as a functional food in anti-inflammation. However, its bioactive components and mechanisms have not been fully elucidated. To discover the bioactive components and anti-inflammatory mechanism, we prepared and separated 8 subfractions from ethyl acetate extract of Chinese propolis (EACP) and investigated the mechanism in oxidized low density lipoprotein (ox-LDL) induced human umbilical vein endothelial cells (HUVECs) damage.

METHODS

Eight subfractions were prepared and separated from ethyl acetate extract of Chinese propolis (EACP) with different concentrations of methanol-water solution, and analysed its chemical constituents by HPLC-DAD/Q-TOF-MS. Then 80% confluent HUVECs were stimulated with 40 μg/mL ox-LDL. Cell viability and apoptosis were evaluated by Sulforhodamine B (SRB) assay and Hoechst 33,258 staining, respectively. Levels of caspase 3, PARP, LC3B, p62, p-mTOR, p-p70S6K, p-PI3K, p-Akt, LOX-1 and p-p38 MAPK were assessed by western blotting and immunofluorescence assay, respectively. Reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were measured with fluorescent probes.

RESULTS

Each subfraction exhibited similar protective effect although the contents of chemical constituents were different. EACP attenuated ox-LDL induced HUVECs apoptosis, depressed the ratio of LC3-II/LC3-I and enhanced the p62 level. In addition, treatment with EACP also activated the phosphorylation of PI3K/Akt/mTOR, and deactivated the level of LOX-1 and phosphorylation of p38 MAPK. The overproduction of ROS and the damage of MMP were also ameliorated after ECAP treatment.

CONCLUSIONS

These findings indicated that the bioactive component of propolis on anti-inflammatory activity was not determined by a single constituent, but a complex interaction including flavonoids, esters and phenolic acids. EACP attenuated ox-LDL induced HUVECs injury by inhibiting LOX-1 level and depressed ROS production against oxidative stress in ox-LDL induced HUVECs, further to activate PI3K/Akt/mTOR pathway and deactivate p38 MAPK to inhibit apoptosis and autophagy, which provide novel insights into the potential application of propolis on modulating chronic inflammation.

DOI: 10.1186/s12906-018-2215-8
PubMed: 29724195
PubMed Central: PMC5934819

Affiliations:

République populaire de Chine

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

to stream Main, to step Corpus: 000E49
to stream Main, to step Curation: 000E49

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (drug effects)</term>
<term>Autophagy (drug effects)</term>
<term>Cell Line (MeSH)</term>
<term>Cell Survival (drug effects)</term>
<term>Chromatography, High Pressure Liquid (MeSH)</term>
<term>Human Umbilical Vein Endothelial Cells (drug effects)</term>
<term>Humans (MeSH)</term>
<term>Lipoproteins, LDL (adverse effects)</term>
<term>Oxidative Stress (drug effects)</term>
<term>Populus (chemistry)</term>
<term>Propolis (pharmacology)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>p38 Mitogen-Activated Protein Kinases (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Apoptose (effets des médicaments et des substances chimiques)</term>
<term>Autophagie (effets des médicaments et des substances chimiques)</term>
<term>Cellules endothéliales de la veine ombilicale humaine (effets des médicaments et des substances chimiques)</term>
<term>Chromatographie en phase liquide à haute performance (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Lipoprotéines LDL (effets indésirables)</term>
<term>Populus (composition chimique)</term>
<term>Propolis (pharmacologie)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Stress oxydatif (effets des médicaments et des substances chimiques)</term>
<term>Survie cellulaire (effets des médicaments et des substances chimiques)</term>
<term>p38 Mitogen-Activated Protein Kinases (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Lipoproteins, LDL</term>
</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Populus</term>
</keywords>
<keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Populus</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>Autophagy</term>
<term>Cell Survival</term>
<term>Human Umbilical Vein Endothelial Cells</term>
<term>Oxidative Stress</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Apoptose</term>
<term>Autophagie</term>
<term>Cellules endothéliales de la veine ombilicale humaine</term>
<term>Stress oxydatif</term>
<term>Survie cellulaire</term>
</keywords>
<keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Lipoprotéines LDL</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Proto-Oncogene Proteins c-akt</term>
<term>p38 Mitogen-Activated Protein Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines proto-oncogènes c-akt</term>
<term>p38 Mitogen-Activated Protein Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Propolis</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Propolis</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line</term>
<term>Chromatography, High Pressure Liquid</term>
<term>Humans</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Chromatographie en phase liquide à haute performance</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>Propolis, a polyphenol-rich natural product, has been used as a functional food in anti-inflammation. However, its bioactive components and mechanisms have not been fully elucidated. To discover the bioactive components and anti-inflammatory mechanism, we prepared and separated 8 subfractions from ethyl acetate extract of Chinese propolis (EACP) and investigated the mechanism in oxidized low density lipoprotein (ox-LDL) induced human umbilical vein endothelial cells (HUVECs) damage.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>Eight subfractions were prepared and separated from ethyl acetate extract of Chinese propolis (EACP) with different concentrations of methanol-water solution, and analysed its chemical constituents by HPLC-DAD/Q-TOF-MS. Then 80% confluent HUVECs were stimulated with 40 μg/mL ox-LDL. Cell viability and apoptosis were evaluated by Sulforhodamine B (SRB) assay and Hoechst 33,258 staining, respectively. Levels of caspase 3, PARP, LC3B, p62, p-mTOR, p-p70S6K, p-PI3K, p-Akt, LOX-1 and p-p38 MAPK were assessed by western blotting and immunofluorescence assay, respectively. Reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were measured with fluorescent probes.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>Each subfraction exhibited similar protective effect although the contents of chemical constituents were different. EACP attenuated ox-LDL induced HUVECs apoptosis, depressed the ratio of LC3-II/LC3-I and enhanced the p62 level. In addition, treatment with EACP also activated the phosphorylation of PI3K/Akt/mTOR, and deactivated the level of LOX-1 and phosphorylation of p38 MAPK. The overproduction of ROS and the damage of MMP were also ameliorated after ECAP treatment.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>These findings indicated that the bioactive component of propolis on anti-inflammatory activity was not determined by a single constituent, but a complex interaction including flavonoids, esters and phenolic acids. EACP attenuated ox-LDL induced HUVECs injury by inhibiting LOX-1 level and depressed ROS production against oxidative stress in ox-LDL induced HUVECs, further to activate PI3K/Akt/mTOR pathway and deactivate p38 MAPK to inhibit apoptosis and autophagy, which provide novel insights into the potential application of propolis on modulating chronic inflammation.</p>
</div>
</front>
</TEI>
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<DateCompleted><Year>2018</Year>
<Month>05</Month>
<Day>25</Day>
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<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>14</Day>
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<Issue>1</Issue>
<PubDate><Year>2018</Year>
<Month>May</Month>
<Day>03</Day>
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<Title>BMC complementary and alternative medicine</Title>
<ISOAbbreviation>BMC Complement Altern Med</ISOAbbreviation>
</Journal>
<ArticleTitle>Bioactive components and mechanisms of Chinese poplar propolis alleviates oxidized low-density lipoprotein-induced endothelial cells injury.</ArticleTitle>
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<ELocationID EIdType="doi" ValidYN="Y">10.1186/s12906-018-2215-8</ELocationID>
<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Propolis, a polyphenol-rich natural product, has been used as a functional food in anti-inflammation. However, its bioactive components and mechanisms have not been fully elucidated. To discover the bioactive components and anti-inflammatory mechanism, we prepared and separated 8 subfractions from ethyl acetate extract of Chinese propolis (EACP) and investigated the mechanism in oxidized low density lipoprotein (ox-LDL) induced human umbilical vein endothelial cells (HUVECs) damage.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Eight subfractions were prepared and separated from ethyl acetate extract of Chinese propolis (EACP) with different concentrations of methanol-water solution, and analysed its chemical constituents by HPLC-DAD/Q-TOF-MS. Then 80% confluent HUVECs were stimulated with 40 μg/mL ox-LDL. Cell viability and apoptosis were evaluated by Sulforhodamine B (SRB) assay and Hoechst 33,258 staining, respectively. Levels of caspase 3, PARP, LC3B, p62, p-mTOR, p-p70S6K, p-PI3K, p-Akt, LOX-1 and p-p38 MAPK were assessed by western blotting and immunofluorescence assay, respectively. Reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were measured with fluorescent probes.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Each subfraction exhibited similar protective effect although the contents of chemical constituents were different. EACP attenuated ox-LDL induced HUVECs apoptosis, depressed the ratio of LC3-II/LC3-I and enhanced the p62 level. In addition, treatment with EACP also activated the phosphorylation of PI3K/Akt/mTOR, and deactivated the level of LOX-1 and phosphorylation of p38 MAPK. The overproduction of ROS and the damage of MMP were also ameliorated after ECAP treatment.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">These findings indicated that the bioactive component of propolis on anti-inflammatory activity was not determined by a single constituent, but a complex interaction including flavonoids, esters and phenolic acids. EACP attenuated ox-LDL induced HUVECs injury by inhibiting LOX-1 level and depressed ROS production against oxidative stress in ox-LDL induced HUVECs, further to activate PI3K/Akt/mTOR pathway and deactivate p38 MAPK to inhibit apoptosis and autophagy, which provide novel insights into the potential application of propolis on modulating chronic inflammation.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chang</LastName>
<ForeName>Huasong</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>School of Life Science, Liaocheng University, Liaocheng, 252059, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yuan</LastName>
<ForeName>Wenwen</ForeName>
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<AffiliationInfo><Affiliation>School of Life Science, Liaocheng University, Liaocheng, 252059, China.</Affiliation>
</AffiliationInfo>
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<ForeName>Haizhu</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>School of Life Science, Liaocheng University, Liaocheng, 252059, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yin</LastName>
<ForeName>Xusheng</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Institute of Apiculture and bee product quality inspection of Shandong Province, Taian, 271000, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xuan</LastName>
<ForeName>Hongzhuan</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>School of Life Science, Liaocheng University, Liaocheng, 252059, China. hongzhuanxuan@163.com.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>31201860, 31672499</GrantID>
<Agency>National Natural Science Foundation of China</Agency>
<Country></Country>
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</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>05</Month>
<Day>03</Day>
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<MedlineJournalInfo><Country>England</Country>
<MedlineTA>BMC Complement Altern Med</MedlineTA>
<NlmUniqueID>101088661</NlmUniqueID>
<ISSNLinking>1472-6882</ISSNLinking>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D008077">Lipoproteins, LDL</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C099252">oxidized low density lipoprotein</NameOfSubstance>
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<Chemical><RegistryNumber>9009-62-5</RegistryNumber>
<NameOfSubstance UI="D011429">Propolis</NameOfSubstance>
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<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance>
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<Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber>
<NameOfSubstance UI="D048051">p38 Mitogen-Activated Protein Kinases</NameOfSubstance>
</Chemical>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002851" MajorTopicYN="N">Chromatography, High Pressure Liquid</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D061307" MajorTopicYN="N">Human Umbilical Vein Endothelial Cells</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
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<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008077" MajorTopicYN="N">Lipoproteins, LDL</DescriptorName>
<QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D032107" MajorTopicYN="N">Populus</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011429" MajorTopicYN="N">Propolis</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
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Bioactive components and mechanisms of Chinese poplar propolis alleviates oxidized low-density lipoprotein-induced endothelial cells injury.

Bioactive components and mechanisms of Chinese poplar propolis alleviates oxidized low-density lipoprotein-induced endothelial cells injury.

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