Treatment of Peroxidase Derived from Foxtail Millet Bran Attenuates Atherosclerosis by Inhibition of CD36 and STAT3 in Vitro and in Vivo.
Identifieur interne : 000011 ( Main/Exploration ); précédent : 000010; suivant : 000012Treatment of Peroxidase Derived from Foxtail Millet Bran Attenuates Atherosclerosis by Inhibition of CD36 and STAT3 in Vitro and in Vivo.
Auteurs : Fengming Liu ; Shuhua Shan ; Hanqing Li ; Zhuoyu LiSource :
- Journal of agricultural and food chemistry [ 1520-5118 ] ; 2020.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Antigènes CD36 (génétique), Antigènes CD36 (métabolisme), Apolipoprotéines E (génétique), Apolipoprotéines E (métabolisme), Athérosclérose (génétique), Athérosclérose (métabolisme), Athérosclérose (traitement médicamenteux), Cellules THP-1 (MeSH), Facteur de transcription STAT-3 (génétique), Facteur de transcription STAT-3 (métabolisme), Humains (MeSH), Myeloperoxidase (administration et posologie), Mâle (MeSH), Protéines végétales (administration et posologie), Setaria (plante) (composition chimique), Setaria (plante) (enzymologie), Souris (MeSH), Souris knockout (MeSH).
- MESH :
- administration et posologie : Myeloperoxidase, Protéines végétales.
- composition chimique : Setaria (plante).
- enzymologie : Setaria (plante).
- génétique : Antigènes CD36, Apolipoprotéines E, Athérosclérose, Facteur de transcription STAT-3.
- métabolisme : Antigènes CD36, Apolipoprotéines E, Athérosclérose, Facteur de transcription STAT-3.
- traitement médicamenteux : Athérosclérose.
- Animaux, Cellules THP-1, Humains, Mâle, Souris, Souris knockout.
English descriptors
- KwdEn :
- Animals (MeSH), Apolipoproteins E (genetics), Apolipoproteins E (metabolism), Atherosclerosis (drug therapy), Atherosclerosis (genetics), Atherosclerosis (metabolism), CD36 Antigens (genetics), CD36 Antigens (metabolism), Humans (MeSH), Male (MeSH), Mice (MeSH), Mice, Knockout (MeSH), Peroxidase (administration & dosage), Plant Proteins (administration & dosage), STAT3 Transcription Factor (genetics), STAT3 Transcription Factor (metabolism), Setaria Plant (chemistry), Setaria Plant (enzymology), THP-1 Cells (MeSH).
- MESH :
- chemical , administration & dosage : Peroxidase, Plant Proteins.
- chemical , genetics : Apolipoproteins E, CD36 Antigens, STAT3 Transcription Factor.
- chemical , metabolism : Apolipoproteins E, CD36 Antigens, STAT3 Transcription Factor.
- chemistry : Setaria Plant.
- drug therapy : Atherosclerosis.
- enzymology : Setaria Plant.
- genetics : Atherosclerosis.
- metabolism : Atherosclerosis.
- Animals, Humans, Male, Mice, Mice, Knockout, THP-1 Cells.
Abstract
Atherosclerosis is one of the main causes of cardiovascular diseases. Our previous study indicated that a type of peroxidase derived from foxtail millet bran (FMBP) had prominent antitumor activities. In the present study, we found that FMBP had potential antiatherosclerosis effects. The results showed that FMBP treatment strongly suppressed lipid phagocytosis in both HASMCs and THP-1 cells by 52% and 49%, respectively. Further, FMBP significantly inhibited HASMCs migration by promoting transformation of HASMCs from synthetic to contractile, leading to the decrease of lipid phagocytosis. Simultaneously, FMBP repressed lipid uptake by reducing the expression of CD36 in THP-1 cells. In addition, FMBP reduced the secretion of inflammatory factor IL-1β by inhibiting the expression of STAT3 in THP-1 cells. Interestingly, FMBP also had the same effects in models of atherosclerosis constructed with ApoE-/- mice, including decreased aortic lesion area, repressed aortic sinus CD36 and STAT3 expression, and elevated serum HDL-C concentration. Collectively, these results indicate that FMBP has great potential in preventing the development of atherosclerosis.
DOI: 10.1021/acs.jafc.9b06963
PubMed: 31965794
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<author><name sortKey="Shan, Shuhua" sort="Shan, Shuhua" uniqKey="Shan S" first="Shuhua" last="Shan">Shuhua Shan</name>
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<author><name sortKey="Li, Hanqing" sort="Li, Hanqing" uniqKey="Li H" first="Hanqing" last="Li">Hanqing Li</name>
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<author><name sortKey="Li, Zhuoyu" sort="Li, Zhuoyu" uniqKey="Li Z" first="Zhuoyu" last="Li">Zhuoyu Li</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Apolipoproteins E (genetics)</term>
<term>Apolipoproteins E (metabolism)</term>
<term>Atherosclerosis (drug therapy)</term>
<term>Atherosclerosis (genetics)</term>
<term>Atherosclerosis (metabolism)</term>
<term>CD36 Antigens (genetics)</term>
<term>CD36 Antigens (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Male (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Peroxidase (administration & dosage)</term>
<term>Plant Proteins (administration & dosage)</term>
<term>STAT3 Transcription Factor (genetics)</term>
<term>STAT3 Transcription Factor (metabolism)</term>
<term>Setaria Plant (chemistry)</term>
<term>Setaria Plant (enzymology)</term>
<term>THP-1 Cells (MeSH)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Antigènes CD36 (génétique)</term>
<term>Antigènes CD36 (métabolisme)</term>
<term>Apolipoprotéines E (génétique)</term>
<term>Apolipoprotéines E (métabolisme)</term>
<term>Athérosclérose (génétique)</term>
<term>Athérosclérose (métabolisme)</term>
<term>Athérosclérose (traitement médicamenteux)</term>
<term>Cellules THP-1 (MeSH)</term>
<term>Facteur de transcription STAT-3 (génétique)</term>
<term>Facteur de transcription STAT-3 (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Myeloperoxidase (administration et posologie)</term>
<term>Mâle (MeSH)</term>
<term>Protéines végétales (administration et posologie)</term>
<term>Setaria (plante) (composition chimique)</term>
<term>Setaria (plante) (enzymologie)</term>
<term>Souris (MeSH)</term>
<term>Souris knockout (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Peroxidase</term>
<term>Plant Proteins</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Apolipoproteins E</term>
<term>CD36 Antigens</term>
<term>STAT3 Transcription Factor</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Apolipoproteins E</term>
<term>CD36 Antigens</term>
<term>STAT3 Transcription Factor</term>
</keywords>
<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Myeloperoxidase</term>
<term>Protéines végétales</term>
</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Setaria Plant</term>
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<keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Setaria (plante)</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Atherosclerosis</term>
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<keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Setaria (plante)</term>
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<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Setaria Plant</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Atherosclerosis</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Antigènes CD36</term>
<term>Apolipoprotéines E</term>
<term>Athérosclérose</term>
<term>Facteur de transcription STAT-3</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Atherosclerosis</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigènes CD36</term>
<term>Apolipoprotéines E</term>
<term>Athérosclérose</term>
<term>Facteur de transcription STAT-3</term>
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<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Athérosclérose</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Humans</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>THP-1 Cells</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules THP-1</term>
<term>Humains</term>
<term>Mâle</term>
<term>Souris</term>
<term>Souris knockout</term>
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<front><div type="abstract" xml:lang="en">Atherosclerosis is one of the main causes of cardiovascular diseases. Our previous study indicated that a type of peroxidase derived from foxtail millet bran (FMBP) had prominent antitumor activities. In the present study, we found that FMBP had potential antiatherosclerosis effects. The results showed that FMBP treatment strongly suppressed lipid phagocytosis in both HASMCs and THP-1 cells by 52% and 49%, respectively. Further, FMBP significantly inhibited HASMCs migration by promoting transformation of HASMCs from synthetic to contractile, leading to the decrease of lipid phagocytosis. Simultaneously, FMBP repressed lipid uptake by reducing the expression of CD36 in THP-1 cells. In addition, FMBP reduced the secretion of inflammatory factor IL-1β by inhibiting the expression of STAT3 in THP-1 cells. Interestingly, FMBP also had the same effects in models of atherosclerosis constructed with ApoE-/- mice, including decreased aortic lesion area, repressed aortic sinus CD36 and STAT3 expression, and elevated serum HDL-C concentration. Collectively, these results indicate that FMBP has great potential in preventing the development of atherosclerosis.</div>
</front>
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<Abstract><AbstractText>Atherosclerosis is one of the main causes of cardiovascular diseases. Our previous study indicated that a type of peroxidase derived from foxtail millet bran (FMBP) had prominent antitumor activities. In the present study, we found that FMBP had potential antiatherosclerosis effects. The results showed that FMBP treatment strongly suppressed lipid phagocytosis in both HASMCs and THP-1 cells by 52% and 49%, respectively. Further, FMBP significantly inhibited HASMCs migration by promoting transformation of HASMCs from synthetic to contractile, leading to the decrease of lipid phagocytosis. Simultaneously, FMBP repressed lipid uptake by reducing the expression of CD36 in THP-1 cells. In addition, FMBP reduced the secretion of inflammatory factor IL-1β by inhibiting the expression of STAT3 in THP-1 cells. Interestingly, FMBP also had the same effects in models of atherosclerosis constructed with ApoE-/- mice, including decreased aortic lesion area, repressed aortic sinus CD36 and STAT3 expression, and elevated serum HDL-C concentration. Collectively, these results indicate that FMBP has great potential in preventing the development of atherosclerosis.</AbstractText>
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