Apigenin Improves Hypertension and Cardiac Hypertrophy Through Modulating NADPH Oxidase-Dependent ROS Generation and Cytokines in Hypothalamic Paraventricular Nucleus
Apigenin, identified as 4′, 5, 7-trihydroxyflavone, is a natural flavonoid compound that has many interesting pharmacological activities and nutraceutical potential including anti-inflammatory and antioxidant functions. Chronic, low-grade inflammation and oxidative stress are involved in both the in...
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| Veröffentlicht in: | Cardiovascular toxicology 2021-09, Vol.21 (9), p.721-736 |
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| creator | Gao, Hong-Li Yu, Xiao-Jing Hu, Han-Bo Yang, Qian-Wen Liu, Kai-Li Chen, Yan-Mei Zhang, Yan Zhang, Dong-Dong Tian, Hua Zhu, Guo-Qing Qi, Jie Kang, Yu-Ming |
| description | Apigenin, identified as 4′, 5, 7-trihydroxyflavone, is a natural flavonoid compound that has many interesting pharmacological activities and nutraceutical potential including anti-inflammatory and antioxidant functions. Chronic, low-grade inflammation and oxidative stress are involved in both the initiation and progression of hypertension and hypertension-induced cardiac hypertrophy. However, whether or not apigenin improves hypertension and cardiac hypertrophy through modulating NADPH oxidase-dependent reactive oxygen species (ROS) generation and inflammation in hypothalamic paraventricular nucleus (PVN) has not been reported. This study aimed to investigate the effects of apigenin on hypertension in spontaneously hypertensive rats (SHRs) and its possible central mechanism of action. SHRs and Wistar-Kyoto (WKY) rats were randomly assigned and treated with bilateral PVN infusion of apigenin or vehicle (artificial cerebrospinal fluid) via osmotic minipumps (20 μg/h) for 4 weeks. The results showed that after PVN infusion of apigenin, the mean arterial pressure (MAP), heart rate, plasma norepinephrine (NE), Beta 1 receptor in kidneys, level of phosphorylation of PKA in the ventricular tissue and cardiac hypertrophy, perivascular fibrosis, heart level of oxidative stress, PVN levels of oxidative stress, interleukin 1β (IL-1β), interleukin 6 (IL-6), iNOS, monocyte chemotactic protein 1 (MCP-1), tyrosine hydroxylase (TH), NOX2 and NOX4 were attenuated and PVN levels of interleukin 10 (IL-10), superoxide dismutase 1 (Cu/Zn-SOD) and the 67-kDa isoform of glutamate decarboxylase (GAD67) were increased. These results revealed that apigenin improves hypertension and cardiac hypertrophy in SHRs which are associated with the down-regulation of NADPH oxidase-dependent ROS generation and inflammation in the PVN. |
| doi_str_mv | 10.1007/s12012-021-09662-1 |
| format | Article |
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Chronic, low-grade inflammation and oxidative stress are involved in both the initiation and progression of hypertension and hypertension-induced cardiac hypertrophy. However, whether or not apigenin improves hypertension and cardiac hypertrophy through modulating NADPH oxidase-dependent reactive oxygen species (ROS) generation and inflammation in hypothalamic paraventricular nucleus (PVN) has not been reported. This study aimed to investigate the effects of apigenin on hypertension in spontaneously hypertensive rats (SHRs) and its possible central mechanism of action. SHRs and Wistar-Kyoto (WKY) rats were randomly assigned and treated with bilateral PVN infusion of apigenin or vehicle (artificial cerebrospinal fluid) via osmotic minipumps (20 μg/h) for 4 weeks. The results showed that after PVN infusion of apigenin, the mean arterial pressure (MAP), heart rate, plasma norepinephrine (NE), Beta 1 receptor in kidneys, level of phosphorylation of PKA in the ventricular tissue and cardiac hypertrophy, perivascular fibrosis, heart level of oxidative stress, PVN levels of oxidative stress, interleukin 1β (IL-1β), interleukin 6 (IL-6), iNOS, monocyte chemotactic protein 1 (MCP-1), tyrosine hydroxylase (TH), NOX2 and NOX4 were attenuated and PVN levels of interleukin 10 (IL-10), superoxide dismutase 1 (Cu/Zn-SOD) and the 67-kDa isoform of glutamate decarboxylase (GAD67) were increased. These results revealed that apigenin improves hypertension and cardiac hypertrophy in SHRs which are associated with the down-regulation of NADPH oxidase-dependent ROS generation and inflammation in the PVN.</description><identifier>ISSN: 1530-7905</identifier><identifier>EISSN: 1559-0259</identifier><identifier>DOI: 10.1007/s12012-021-09662-1</identifier><identifier>PMID: 34076830</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Anti-Inflammatory Agents - pharmacology ; Antihypertensive Agents - pharmacology ; Antioxidants ; Antioxidants - pharmacology ; Apigenin - pharmacology ; Arterial Pressure - drug effects ; Bioflavonoids ; Biomedical and Life Sciences ; Biomedicine ; Blood pressure ; Brain ; Cardiology ; Cardiomegaly - drug therapy ; Cardiomegaly - enzymology ; Cardiomegaly - physiopathology ; Cerebrospinal fluid ; CYBB protein ; Cytokines ; Cytokines - metabolism ; Disease Models, Animal ; Down-regulation ; Fibrosis ; Flavones ; Flavonoids ; Functional foods & nutraceuticals ; Glutamate decarboxylase ; Heart ; Heart beat ; Heart enlargement ; Heart rate ; Hydroxylase ; Hypertension ; Hypertension - drug therapy ; Hypertension - enzymology ; Hypertension - physiopathology ; Hypertrophy ; Hypothalamus ; Inflammation ; Interleukin 10 ; Interleukin 6 ; Interleukins ; Kidneys ; Male ; Monocyte chemoattractant protein 1 ; Monocytes ; Myocardium - metabolism ; Myocardium - pathology ; NAD(P)H oxidase ; NADPH Oxidases - genetics ; NADPH Oxidases - metabolism ; Nitric-oxide synthase ; Norepinephrine ; Oxidases ; Oxidation ; Oxidative stress ; Oxidative Stress - drug effects ; Paraventricular Hypothalamic Nucleus - drug effects ; Paraventricular Hypothalamic Nucleus - enzymology ; Paraventricular Hypothalamic Nucleus - physiopathology ; Pharmacology/Toxicology ; Phosphorylation ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Superoxide ; Superoxide dismutase ; Tyrosine ; Ventricle ; Ventricular Function, Left - drug effects ; Ventricular Remodeling - drug effects</subject><ispartof>Cardiovascular toxicology, 2021-09, Vol.21 (9), p.721-736</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>COPYRIGHT 2021 Springer</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-804ae09e0943a620c94b7b0d29aa86847318b1c511cc29389ede94b50722146c3</citedby><cites>FETCH-LOGICAL-c442t-804ae09e0943a620c94b7b0d29aa86847318b1c511cc29389ede94b50722146c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12012-021-09662-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12012-021-09662-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34076830$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gao, Hong-Li</creatorcontrib><creatorcontrib>Yu, Xiao-Jing</creatorcontrib><creatorcontrib>Hu, Han-Bo</creatorcontrib><creatorcontrib>Yang, Qian-Wen</creatorcontrib><creatorcontrib>Liu, Kai-Li</creatorcontrib><creatorcontrib>Chen, Yan-Mei</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Zhang, Dong-Dong</creatorcontrib><creatorcontrib>Tian, Hua</creatorcontrib><creatorcontrib>Zhu, Guo-Qing</creatorcontrib><creatorcontrib>Qi, Jie</creatorcontrib><creatorcontrib>Kang, Yu-Ming</creatorcontrib><title>Apigenin Improves Hypertension and Cardiac Hypertrophy Through Modulating NADPH Oxidase-Dependent ROS Generation and Cytokines in Hypothalamic Paraventricular Nucleus</title><title>Cardiovascular toxicology</title><addtitle>Cardiovasc Toxicol</addtitle><addtitle>Cardiovasc Toxicol</addtitle><description>Apigenin, identified as 4′, 5, 7-trihydroxyflavone, is a natural flavonoid compound that has many interesting pharmacological activities and nutraceutical potential including anti-inflammatory and antioxidant functions. Chronic, low-grade inflammation and oxidative stress are involved in both the initiation and progression of hypertension and hypertension-induced cardiac hypertrophy. However, whether or not apigenin improves hypertension and cardiac hypertrophy through modulating NADPH oxidase-dependent reactive oxygen species (ROS) generation and inflammation in hypothalamic paraventricular nucleus (PVN) has not been reported. This study aimed to investigate the effects of apigenin on hypertension in spontaneously hypertensive rats (SHRs) and its possible central mechanism of action. SHRs and Wistar-Kyoto (WKY) rats were randomly assigned and treated with bilateral PVN infusion of apigenin or vehicle (artificial cerebrospinal fluid) via osmotic minipumps (20 μg/h) for 4 weeks. The results showed that after PVN infusion of apigenin, the mean arterial pressure (MAP), heart rate, plasma norepinephrine (NE), Beta 1 receptor in kidneys, level of phosphorylation of PKA in the ventricular tissue and cardiac hypertrophy, perivascular fibrosis, heart level of oxidative stress, PVN levels of oxidative stress, interleukin 1β (IL-1β), interleukin 6 (IL-6), iNOS, monocyte chemotactic protein 1 (MCP-1), tyrosine hydroxylase (TH), NOX2 and NOX4 were attenuated and PVN levels of interleukin 10 (IL-10), superoxide dismutase 1 (Cu/Zn-SOD) and the 67-kDa isoform of glutamate decarboxylase (GAD67) were increased. These results revealed that apigenin improves hypertension and cardiac hypertrophy in SHRs which are associated with the down-regulation of NADPH oxidase-dependent ROS generation and inflammation in the PVN.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Apigenin - pharmacology</subject><subject>Arterial Pressure - drug effects</subject><subject>Bioflavonoids</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood pressure</subject><subject>Brain</subject><subject>Cardiology</subject><subject>Cardiomegaly - drug therapy</subject><subject>Cardiomegaly - enzymology</subject><subject>Cardiomegaly - physiopathology</subject><subject>Cerebrospinal fluid</subject><subject>CYBB protein</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Down-regulation</subject><subject>Fibrosis</subject><subject>Flavones</subject><subject>Flavonoids</subject><subject>Functional foods & nutraceuticals</subject><subject>Glutamate decarboxylase</subject><subject>Heart</subject><subject>Heart beat</subject><subject>Heart enlargement</subject><subject>Heart rate</subject><subject>Hydroxylase</subject><subject>Hypertension</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - enzymology</subject><subject>Hypertension - physiopathology</subject><subject>Hypertrophy</subject><subject>Hypothalamus</subject><subject>Inflammation</subject><subject>Interleukin 10</subject><subject>Interleukin 6</subject><subject>Interleukins</subject><subject>Kidneys</subject><subject>Male</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>NAD(P)H oxidase</subject><subject>NADPH Oxidases - genetics</subject><subject>NADPH Oxidases - metabolism</subject><subject>Nitric-oxide synthase</subject><subject>Norepinephrine</subject><subject>Oxidases</subject><subject>Oxidation</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Paraventricular Hypothalamic Nucleus - drug effects</subject><subject>Paraventricular Hypothalamic Nucleus - enzymology</subject><subject>Paraventricular Hypothalamic Nucleus - 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pharmacology</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Apigenin - pharmacology</topic><topic>Arterial Pressure - drug effects</topic><topic>Bioflavonoids</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood pressure</topic><topic>Brain</topic><topic>Cardiology</topic><topic>Cardiomegaly - drug therapy</topic><topic>Cardiomegaly - enzymology</topic><topic>Cardiomegaly - physiopathology</topic><topic>Cerebrospinal fluid</topic><topic>CYBB protein</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Down-regulation</topic><topic>Fibrosis</topic><topic>Flavones</topic><topic>Flavonoids</topic><topic>Functional foods & nutraceuticals</topic><topic>Glutamate decarboxylase</topic><topic>Heart</topic><topic>Heart beat</topic><topic>Heart enlargement</topic><topic>Heart rate</topic><topic>Hydroxylase</topic><topic>Hypertension</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - enzymology</topic><topic>Hypertension - physiopathology</topic><topic>Hypertrophy</topic><topic>Hypothalamus</topic><topic>Inflammation</topic><topic>Interleukin 10</topic><topic>Interleukin 6</topic><topic>Interleukins</topic><topic>Kidneys</topic><topic>Male</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Monocytes</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>NAD(P)H oxidase</topic><topic>NADPH Oxidases - genetics</topic><topic>NADPH Oxidases - metabolism</topic><topic>Nitric-oxide synthase</topic><topic>Norepinephrine</topic><topic>Oxidases</topic><topic>Oxidation</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Paraventricular Hypothalamic Nucleus - drug effects</topic><topic>Paraventricular Hypothalamic Nucleus - enzymology</topic><topic>Paraventricular Hypothalamic Nucleus - physiopathology</topic><topic>Pharmacology/Toxicology</topic><topic>Phosphorylation</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Superoxide</topic><topic>Superoxide dismutase</topic><topic>Tyrosine</topic><topic>Ventricle</topic><topic>Ventricular Function, Left - drug effects</topic><topic>Ventricular Remodeling - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gao, Hong-Li</creatorcontrib><creatorcontrib>Yu, Xiao-Jing</creatorcontrib><creatorcontrib>Hu, Han-Bo</creatorcontrib><creatorcontrib>Yang, Qian-Wen</creatorcontrib><creatorcontrib>Liu, Kai-Li</creatorcontrib><creatorcontrib>Chen, Yan-Mei</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Zhang, Dong-Dong</creatorcontrib><creatorcontrib>Tian, Hua</creatorcontrib><creatorcontrib>Zhu, Guo-Qing</creatorcontrib><creatorcontrib>Qi, Jie</creatorcontrib><creatorcontrib>Kang, Yu-Ming</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Cardiovascular toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gao, Hong-Li</au><au>Yu, Xiao-Jing</au><au>Hu, Han-Bo</au><au>Yang, Qian-Wen</au><au>Liu, Kai-Li</au><au>Chen, Yan-Mei</au><au>Zhang, Yan</au><au>Zhang, Dong-Dong</au><au>Tian, Hua</au><au>Zhu, Guo-Qing</au><au>Qi, Jie</au><au>Kang, Yu-Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apigenin Improves Hypertension and Cardiac Hypertrophy Through Modulating NADPH Oxidase-Dependent ROS Generation and Cytokines in Hypothalamic Paraventricular Nucleus</atitle><jtitle>Cardiovascular toxicology</jtitle><stitle>Cardiovasc Toxicol</stitle><addtitle>Cardiovasc Toxicol</addtitle><date>2021-09-01</date><risdate>2021</risdate><volume>21</volume><issue>9</issue><spage>721</spage><epage>736</epage><pages>721-736</pages><issn>1530-7905</issn><eissn>1559-0259</eissn><abstract>Apigenin, identified as 4′, 5, 7-trihydroxyflavone, is a natural flavonoid compound that has many interesting pharmacological activities and nutraceutical potential including anti-inflammatory and antioxidant functions. Chronic, low-grade inflammation and oxidative stress are involved in both the initiation and progression of hypertension and hypertension-induced cardiac hypertrophy. However, whether or not apigenin improves hypertension and cardiac hypertrophy through modulating NADPH oxidase-dependent reactive oxygen species (ROS) generation and inflammation in hypothalamic paraventricular nucleus (PVN) has not been reported. This study aimed to investigate the effects of apigenin on hypertension in spontaneously hypertensive rats (SHRs) and its possible central mechanism of action. SHRs and Wistar-Kyoto (WKY) rats were randomly assigned and treated with bilateral PVN infusion of apigenin or vehicle (artificial cerebrospinal fluid) via osmotic minipumps (20 μg/h) for 4 weeks. The results showed that after PVN infusion of apigenin, the mean arterial pressure (MAP), heart rate, plasma norepinephrine (NE), Beta 1 receptor in kidneys, level of phosphorylation of PKA in the ventricular tissue and cardiac hypertrophy, perivascular fibrosis, heart level of oxidative stress, PVN levels of oxidative stress, interleukin 1β (IL-1β), interleukin 6 (IL-6), iNOS, monocyte chemotactic protein 1 (MCP-1), tyrosine hydroxylase (TH), NOX2 and NOX4 were attenuated and PVN levels of interleukin 10 (IL-10), superoxide dismutase 1 (Cu/Zn-SOD) and the 67-kDa isoform of glutamate decarboxylase (GAD67) were increased. These results revealed that apigenin improves hypertension and cardiac hypertrophy in SHRs which are associated with the down-regulation of NADPH oxidase-dependent ROS generation and inflammation in the PVN.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34076830</pmid><doi>10.1007/s12012-021-09662-1</doi><tpages>16</tpages></addata></record> |
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| ispartof | Cardiovascular toxicology, 2021-09, Vol.21 (9), p.721-736 |
| issn | 1530-7905 1559-0259 |
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| recordid | cdi_proquest_miscellaneous_2536484425 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Animals Anti-Inflammatory Agents - pharmacology Antihypertensive Agents - pharmacology Antioxidants Antioxidants - pharmacology Apigenin - pharmacology Arterial Pressure - drug effects Bioflavonoids Biomedical and Life Sciences Biomedicine Blood pressure Brain Cardiology Cardiomegaly - drug therapy Cardiomegaly - enzymology Cardiomegaly - physiopathology Cerebrospinal fluid CYBB protein Cytokines Cytokines - metabolism Disease Models, Animal Down-regulation Fibrosis Flavones Flavonoids Functional foods & nutraceuticals Glutamate decarboxylase Heart Heart beat Heart enlargement Heart rate Hydroxylase Hypertension Hypertension - drug therapy Hypertension - enzymology Hypertension - physiopathology Hypertrophy Hypothalamus Inflammation Interleukin 10 Interleukin 6 Interleukins Kidneys Male Monocyte chemoattractant protein 1 Monocytes Myocardium - metabolism Myocardium - pathology NAD(P)H oxidase NADPH Oxidases - genetics NADPH Oxidases - metabolism Nitric-oxide synthase Norepinephrine Oxidases Oxidation Oxidative stress Oxidative Stress - drug effects Paraventricular Hypothalamic Nucleus - drug effects Paraventricular Hypothalamic Nucleus - enzymology Paraventricular Hypothalamic Nucleus - physiopathology Pharmacology/Toxicology Phosphorylation Rats Rats, Inbred SHR Rats, Inbred WKY Reactive oxygen species Reactive Oxygen Species - metabolism Superoxide Superoxide dismutase Tyrosine Ventricle Ventricular Function, Left - drug effects Ventricular Remodeling - drug effects |
| title | Apigenin Improves Hypertension and Cardiac Hypertrophy Through Modulating NADPH Oxidase-Dependent ROS Generation and Cytokines in Hypothalamic Paraventricular Nucleus |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-17T17%3A33%3A15IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Apigenin%20Improves%20Hypertension%20and%20Cardiac%20Hypertrophy%20Through%20Modulating%20NADPH%20Oxidase-Dependent%20ROS%20Generation%20and%20Cytokines%20in%20Hypothalamic%20Paraventricular%20Nucleus&rft.jtitle=Cardiovascular%20toxicology&rft.au=Gao,%20Hong-Li&rft.date=2021-09-01&rft.volume=21&rft.issue=9&rft.spage=721&rft.epage=736&rft.pages=721-736&rft.issn=1530-7905&rft.eissn=1559-0259&rft_id=info:doi/10.1007/s12012-021-09662-1&rft_dat=%3Cgale_proqu%3EA706387858%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2554499902&rft_id=info:pmid/34076830&rft_galeid=A706387858&rfr_iscdi=true |