The protective effect of cordyceps sinensis extract on cerebral ischemic injury via modulating the mitochondrial respiratory chain and inhibiting the mitochondrial apoptotic pathway.
Identifieur interne : 000006 ( Main/Exploration ); précédent : 000005; suivant : 000007The protective effect of cordyceps sinensis extract on cerebral ischemic injury via modulating the mitochondrial respiratory chain and inhibiting the mitochondrial apoptotic pathway.
Auteurs : Xue Bai [République populaire de Chine] ; Tian-Yang Tan [République populaire de Chine] ; Yun-Xin Li [République populaire de Chine] ; Yue Li [République populaire de Chine] ; Ya-Fei Chen [République populaire de Chine] ; Ru Ma [République populaire de Chine] ; Shu-Yan Wang [République populaire de Chine] ; Qiang Li [République populaire de Chine] ; Zhen-Quan Liu [République populaire de Chine]Source :
- Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie [ 1950-6007 ] ; 2020.
Descripteurs français
- KwdFr :
- Accident vasculaire cérébral (physiopathologie), Accident vasculaire cérébral (prévention et contrôle), Animaux (MeSH), Apoptose (effets des médicaments et des substances chimiques), Cordyceps (composition chimique), Encéphalopathie ischémique (physiopathologie), Encéphalopathie ischémique (prévention et contrôle), Extraits de plantes (pharmacologie), Infarctus du territoire de l'artère cérébrale moyenne (MeSH), Mitochondries (effets des médicaments et des substances chimiques), Mitochondries (métabolisme), Modèles animaux de maladie humaine (MeSH), Mâle (MeSH), Neuroprotecteurs (isolement et purification), Neuroprotecteurs (pharmacologie), Potentiel de membrane mitochondriale (effets des médicaments et des substances chimiques), Rat Sprague-Dawley (MeSH), Souris (MeSH), Transport d'électrons (effets des médicaments et des substances chimiques).
- MESH :
- composition chimique : Cordyceps.
- effets des médicaments et des substances chimiques : Apoptose, Mitochondries, Potentiel de membrane mitochondriale, Transport d'électrons.
- isolement et purification : Neuroprotecteurs.
- métabolisme : Mitochondries.
- pharmacologie : Extraits de plantes, Neuroprotecteurs.
- physiopathologie : Accident vasculaire cérébral, Encéphalopathie ischémique.
- prévention et contrôle : Accident vasculaire cérébral, Encéphalopathie ischémique.
- Animaux, Infarctus du territoire de l'artère cérébrale moyenne, Modèles animaux de maladie humaine, Mâle, Rat Sprague-Dawley, Souris.
English descriptors
- KwdEn :
- Animals (MeSH), Apoptosis (drug effects), Brain Ischemia (physiopathology), Brain Ischemia (prevention & control), Cordyceps (chemistry), Disease Models, Animal (MeSH), Electron Transport (drug effects), Infarction, Middle Cerebral Artery (MeSH), Male (MeSH), Membrane Potential, Mitochondrial (drug effects), Mice (MeSH), Mitochondria (drug effects), Mitochondria (metabolism), Neuroprotective Agents (isolation & purification), Neuroprotective Agents (pharmacology), Plant Extracts (pharmacology), Rats, Sprague-Dawley (MeSH), Stroke (physiopathology), Stroke (prevention & control).
- MESH :
- chemical , isolation & purification : Neuroprotective Agents.
- chemistry : Cordyceps.
- drug effects : Apoptosis, Electron Transport, Membrane Potential, Mitochondrial, Mitochondria.
- metabolism : Mitochondria.
- chemical , pharmacology : Neuroprotective Agents, Plant Extracts.
- physiopathology : Brain Ischemia, Stroke.
- prevention & control : Brain Ischemia, Stroke.
- Animals, Disease Models, Animal, Infarction, Middle Cerebral Artery, Male, Mice, Rats, Sprague-Dawley.
Abstract
Cerebral ischemia is a common refractory brain disease, resulting from a reduction in the blood flow to the brain. Mitochondrial dysfunction leads to ischemic stroke and brain injury. Cordyceps sinensis (CS) is an important traditional Chinese medicine, which has been linked to neuroprotection in recent studies. In this study, we investigated the role of the mitochondrial respiratory chain and the mitochondrial apoptotic pathway on the protective effect of Cordyceps sinensis extract (CSE) against cerebral ischemia injury both in vivo and in vitro. In a murine middle cerebral artery occlusion (MCAO) model, administration of CSE relieved neuronal morphological damage and attenuated the neuronal apoptosis. CSE also reduced neurobehavioral scores and oxygen free radical (OFR), while improving the levels of ATP, cytochrome c oxidase (COX), and mitochondrial complexes I-IV. Furthermore, the mRNA expression of Bax, cytochrome c (Cyt c) and caspase-3 were down-regulated. In brain microvascular endothelial cells (BMECs) exposed to oxygen and glucose deprivation (OGD), CSE prevented OGD-induced cellular apoptosis, and recovered the reduction of mitochondrial membrane potential (MMP). Moreover, CSE treatment induced an increase of Bcl-2 protein expression and a decrease of Bax, Cyt c and caspase-3 protein expression. Meanwhile, the caspase-3, -8, and -9 activities were also inhibited. The results indicate that CSE can relieve cerebral ischemia injury and exhibit protective effects via modulating the mitochondrial respiratory chain and inhibiting the mitochondrial apoptotic pathway.
DOI: 10.1016/j.biopha.2020.109834
PubMed: 31978767
Affiliations:
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Le document en format XML
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sinensis extract on cerebral ischemic injury via modulating the mitochondrial respiratory chain and inhibiting the mitochondrial apoptotic pathway.</title><author><name sortKey="Bai, Xue" sort="Bai, Xue" uniqKey="Bai X" first="Xue" last="Bai">Xue Bai</name><affiliation wicri:level="1"><nlm:affiliation>Chinese Materia Medica School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Chinese Materia Medica School, Beijing University of Chinese Medicine, Beijing 100029</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Tan, Tian Yang" sort="Tan, Tian Yang" uniqKey="Tan T" first="Tian-Yang" last="Tan">Tian-Yang Tan</name><affiliation wicri:level="1"><nlm:affiliation>Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing 100029</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Li, Yun Xin" sort="Li, Yun Xin" uniqKey="Li Y" first="Yun-Xin" last="Li">Yun-Xin Li</name><affiliation wicri:level="1"><nlm:affiliation>Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing 100029</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Li, Yue" sort="Li, Yue" uniqKey="Li Y" first="Yue" last="Li">Yue Li</name><affiliation wicri:level="1"><nlm:affiliation>Chinese Materia Medica School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Chinese Materia Medica School, Beijing University of Chinese Medicine, Beijing 100029</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Chen, Ya Fei" sort="Chen, Ya Fei" uniqKey="Chen Y" first="Ya-Fei" last="Chen">Ya-Fei Chen</name><affiliation wicri:level="1"><nlm:affiliation>Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing 100029</wicri:regionArea><placeName><settlement 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University of Chinese Medicine, Beijing 100029, People's Republic of China. Electronic address: lzqbzy@sina.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Chinese Materia Medica School, Beijing University of Chinese Medicine, Beijing 100029</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author></analytic><series><title level="j">Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie</title><idno type="eISSN">1950-6007</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Apoptosis (drug effects)</term><term>Brain Ischemia (physiopathology)</term><term>Brain Ischemia (prevention & control)</term><term>Cordyceps (chemistry)</term><term>Disease Models, Animal (MeSH)</term><term>Electron Transport (drug effects)</term><term>Infarction, Middle Cerebral Artery (MeSH)</term><term>Male (MeSH)</term><term>Membrane Potential, Mitochondrial (drug effects)</term><term>Mice (MeSH)</term><term>Mitochondria (drug effects)</term><term>Mitochondria (metabolism)</term><term>Neuroprotective Agents (isolation & purification)</term><term>Neuroprotective Agents (pharmacology)</term><term>Plant Extracts (pharmacology)</term><term>Rats, Sprague-Dawley (MeSH)</term><term>Stroke (physiopathology)</term><term>Stroke (prevention & control)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Accident vasculaire cérébral (physiopathologie)</term><term>Accident vasculaire cérébral (prévention et contrôle)</term><term>Animaux (MeSH)</term><term>Apoptose (effets des médicaments et des substances chimiques)</term><term>Cordyceps (composition chimique)</term><term>Encéphalopathie ischémique (physiopathologie)</term><term>Encéphalopathie ischémique (prévention et contrôle)</term><term>Extraits de plantes (pharmacologie)</term><term>Infarctus du territoire de l'artère cérébrale moyenne (MeSH)</term><term>Mitochondries (effets des médicaments et des substances chimiques)</term><term>Mitochondries (métabolisme)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Mâle (MeSH)</term><term>Neuroprotecteurs (isolement et purification)</term><term>Neuroprotecteurs (pharmacologie)</term><term>Potentiel de membrane mitochondriale (effets des médicaments et des substances chimiques)</term><term>Rat Sprague-Dawley (MeSH)</term><term>Souris (MeSH)</term><term>Transport d'électrons (effets des médicaments et des substances chimiques)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="isolation & purification" xml:lang="en"><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Cordyceps</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Cordyceps</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Electron Transport</term><term>Membrane Potential, Mitochondrial</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Apoptose</term><term>Mitochondries</term><term>Potentiel de membrane mitochondriale</term><term>Transport d'électrons</term></keywords><keywords scheme="MESH" qualifier="isolement et purification" xml:lang="fr"><term>Neuroprotecteurs</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Mitochondries</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Extraits de plantes</term><term>Neuroprotecteurs</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Neuroprotective Agents</term><term>Plant Extracts</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Accident vasculaire cérébral</term><term>Encéphalopathie ischémique</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain Ischemia</term><term>Stroke</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Brain Ischemia</term><term>Stroke</term></keywords><keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Accident vasculaire cérébral</term><term>Encéphalopathie ischémique</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Infarction, Middle Cerebral Artery</term><term>Male</term><term>Mice</term><term>Rats, Sprague-Dawley</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Infarctus du territoire de l'artère cérébrale moyenne</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Rat Sprague-Dawley</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cerebral ischemia is a common refractory brain disease, resulting from a reduction in the blood flow to the brain. Mitochondrial dysfunction leads to ischemic stroke and brain injury. Cordyceps sinensis (CS) is an important traditional Chinese medicine, which has been linked to neuroprotection in recent studies. In this study, we investigated the role of the mitochondrial respiratory chain and the mitochondrial apoptotic pathway on the protective effect of Cordyceps sinensis extract (CSE) against cerebral ischemia injury both in vivo and in vitro. In a murine middle cerebral artery occlusion (MCAO) model, administration of CSE relieved neuronal morphological damage and attenuated the neuronal apoptosis. CSE also reduced neurobehavioral scores and oxygen free radical (OFR), while improving the levels of ATP, cytochrome c oxidase (COX), and mitochondrial complexes I-IV. Furthermore, the mRNA expression of Bax, cytochrome c (Cyt c) and caspase-3 were down-regulated. In brain microvascular endothelial cells (BMECs) exposed to oxygen and glucose deprivation (OGD), CSE prevented OGD-induced cellular apoptosis, and recovered the reduction of mitochondrial membrane potential (MMP). Moreover, CSE treatment induced an increase of Bcl-2 protein expression and a decrease of Bax, Cyt c and caspase-3 protein expression. Meanwhile, the caspase-3, -8, and -9 activities were also inhibited. The results indicate that CSE can relieve cerebral ischemia injury and exhibit protective effects via modulating the mitochondrial respiratory chain and inhibiting the mitochondrial apoptotic pathway.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31978767</PMID><DateCompleted><Year>2020</Year><Month>11</Month><Day>20</Day></DateCompleted><DateRevised><Year>2020</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1950-6007</ISSN><JournalIssue CitedMedium="Internet"><Volume>124</Volume><PubDate><Year>2020</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie</Title><ISOAbbreviation>Biomed Pharmacother</ISOAbbreviation></Journal><ArticleTitle>The protective effect of cordyceps sinensis extract on cerebral ischemic injury via modulating the mitochondrial respiratory chain and inhibiting the mitochondrial apoptotic pathway.</ArticleTitle><Pagination><MedlinePgn>109834</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0753-3322(20)30024-X</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.biopha.2020.109834</ELocationID><Abstract><AbstractText>Cerebral ischemia is a common refractory brain disease, resulting from a reduction in the blood flow to the brain. Mitochondrial dysfunction leads to ischemic stroke and brain injury. Cordyceps sinensis (CS) is an important traditional Chinese medicine, which has been linked to neuroprotection in recent studies. In this study, we investigated the role of the mitochondrial respiratory chain and the mitochondrial apoptotic pathway on the protective effect of Cordyceps sinensis extract (CSE) against cerebral ischemia injury both in vivo and in vitro. In a murine middle cerebral artery occlusion (MCAO) model, administration of CSE relieved neuronal morphological damage and attenuated the neuronal apoptosis. CSE also reduced neurobehavioral scores and oxygen free radical (OFR), while improving the levels of ATP, cytochrome c oxidase (COX), and mitochondrial complexes I-IV. Furthermore, the mRNA expression of Bax, cytochrome c (Cyt c) and caspase-3 were down-regulated. In brain microvascular endothelial cells (BMECs) exposed to oxygen and glucose deprivation (OGD), CSE prevented OGD-induced cellular apoptosis, and recovered the reduction of mitochondrial membrane potential (MMP). Moreover, CSE treatment induced an increase of Bcl-2 protein expression and a decrease of Bax, Cyt c and caspase-3 protein expression. Meanwhile, the caspase-3, -8, and -9 activities were also inhibited. The results indicate that CSE can relieve cerebral ischemia injury and exhibit protective effects via modulating the mitochondrial respiratory chain and inhibiting the mitochondrial apoptotic pathway.</AbstractText><CopyrightInformation>Copyright © 2020. Published by Elsevier Masson SAS.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bai</LastName><ForeName>Xue</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Chinese Materia Medica School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Tian-Yang</ForeName><Initials>TY</Initials><AffiliationInfo><Affiliation>Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yun-Xin</ForeName><Initials>YX</Initials><AffiliationInfo><Affiliation>Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yue</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Chinese Materia Medica School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Ya-Fei</ForeName><Initials>YF</Initials><AffiliationInfo><Affiliation>Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Ru</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Chinese Materia Medica School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Shu-Yan</ForeName><Initials>SY</Initials><AffiliationInfo><Affiliation>Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Qiang</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Chinese Materia Medica School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Zhen-Quan</ForeName><Initials>ZQ</Initials><AffiliationInfo><Affiliation>Chinese Materia Medica School, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China. Electronic address: lzqbzy@sina.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>01</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Biomed Pharmacother</MedlineTA><NlmUniqueID>8213295</NlmUniqueID><ISSNLinking>0753-3322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018696">Neuroprotective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010936">Plant Extracts</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002545" MajorTopicYN="N">Brain Ischemia</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D032661" MajorTopicYN="N">Cordyceps</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004579" MajorTopicYN="N">Electron Transport</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020244" MajorTopicYN="N">Infarction, Middle Cerebral Artery</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053078" MajorTopicYN="N">Membrane Potential, Mitochondrial</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018696" MajorTopicYN="N">Neuroprotective Agents</DescriptorName><QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010936" MajorTopicYN="N">Plant Extracts</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020521" MajorTopicYN="N">Stroke</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cerebral is chemic injury</Keyword><Keyword MajorTopicYN="N">Cordyceps sinensis</Keyword><Keyword MajorTopicYN="N">Mitochondrial apoptotic pathway</Keyword><Keyword MajorTopicYN="N">Mitochondrial respiratory chain</Keyword></KeywordList><CoiStatement>Declaration of Competing Interest The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>09</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>12</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>12</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>1</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>11</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>1</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31978767</ArticleId><ArticleId IdType="pii">S0753-3322(20)30024-X</ArticleId><ArticleId IdType="doi">10.1016/j.biopha.2020.109834</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Pékin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Bai, Xue" sort="Bai, Xue" uniqKey="Bai X" first="Xue" last="Bai">Xue Bai</name></noRegion><name sortKey="Chen, Ya Fei" sort="Chen, Ya Fei" uniqKey="Chen Y" first="Ya-Fei" last="Chen">Ya-Fei Chen</name><name sortKey="Li, Qiang" sort="Li, Qiang" uniqKey="Li Q" first="Qiang" last="Li">Qiang Li</name><name sortKey="Li, Yue" sort="Li, Yue" uniqKey="Li Y" first="Yue" last="Li">Yue Li</name><name sortKey="Li, Yun Xin" sort="Li, Yun Xin" uniqKey="Li Y" first="Yun-Xin" last="Li">Yun-Xin Li</name><name sortKey="Liu, Zhen Quan" sort="Liu, Zhen Quan" uniqKey="Liu Z" first="Zhen-Quan" last="Liu">Zhen-Quan Liu</name><name sortKey="Ma, Ru" sort="Ma, Ru" uniqKey="Ma R" first="Ru" last="Ma">Ru Ma</name><name sortKey="Tan, Tian Yang" sort="Tan, Tian Yang" uniqKey="Tan T" first="Tian-Yang" last="Tan">Tian-Yang Tan</name><name sortKey="Wang, Shu Yan" sort="Wang, Shu Yan" uniqKey="Wang S" first="Shu-Yan" last="Wang">Shu-Yan Wang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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