Promoting effect of baicalin on nitric oxide production in CMECs via activating the PI3K-AKT-eNOS pathway attenuates myocardial ischemia–reperfusion injury
Baicalin, which is isolated from Scutellariae Radix, has been shown to possess therapeutic potential for different diseases. Cardiac microvessel injury in myocardial ischemia–reperfusion (IR) has been extensively explored. However, there have been no studies investigating the physiological regulator...
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| creator | Bai, Jiannan Wang, Qingchao Qi, Jiaxin Yu, Hongqiang Wang, Cong Wang, Xiaowei Ren, Yanru Yang, Fude |
| description | Baicalin, which is isolated from Scutellariae Radix, has been shown to possess therapeutic potential for different diseases. Cardiac microvessel injury in myocardial ischemia–reperfusion (IR) has been extensively explored. However, there have been no studies investigating the physiological regulatory mechanisms of baicalin on nitric oxide production and the necroptosis of cardiac microvascular endothelial cells (CMECs) in myocardial IR injury. This study was designed to investigate the contribution of baicalin to repressing necroptosis and preventing IR-mediated CMEC dysfunction.
Indicators of ventricular structure and function were measured by an echocardiographic system. An MTT assay was performed to assess cell viability. Nitrite detection was performed to detect nitric oxide content, and cGMP content was determined using a commercially available cGMP complete ELISA kit. Morphology and molecular characteristics were detected by electron micrographs, quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting.
Our results demonstrated that baicalin significantly improved cardiac function, decreased the myocardial infarction area, and inhibited myocardial cell apoptosis. Moreover, baicalin had a protective effect on cardiac microvessels and promoted the production of nitric oxide (NO) and the level of cGMP in rats that underwent myocardial IR injury. The results of the in vitro experiments showed that baicalin markedly improved cell activity and function in CMECs exposed to hypoxia-reoxygenation (HR). Further experiments indicated that baicalin supplementation suppressed the protein expression of RIP1, RIP3 and p-MLKL to interrupt CMEC necroptosis. In addition, baicalin promoted the production of NO via activating the PI3K-AKT-eNOS signaling pathway. Taken together, our results identified the PI3K-AKT-eNOS axis as a new pathway responsible for reperfusion-mediated microvascular damage.
Baicalin protected CMECs in IR rats by promoting the release of NO via the PI3K-AKT-eNOS pathway and mitigated necroptosis by inhibiting the protein expression of RIP1, RIP3 and p-MLKL.
[Display omitted] |
| doi_str_mv | 10.1016/j.phymed.2019.153035 |
| format | Article |
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Indicators of ventricular structure and function were measured by an echocardiographic system. An MTT assay was performed to assess cell viability. Nitrite detection was performed to detect nitric oxide content, and cGMP content was determined using a commercially available cGMP complete ELISA kit. Morphology and molecular characteristics were detected by electron micrographs, quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting.
Our results demonstrated that baicalin significantly improved cardiac function, decreased the myocardial infarction area, and inhibited myocardial cell apoptosis. Moreover, baicalin had a protective effect on cardiac microvessels and promoted the production of nitric oxide (NO) and the level of cGMP in rats that underwent myocardial IR injury. The results of the in vitro experiments showed that baicalin markedly improved cell activity and function in CMECs exposed to hypoxia-reoxygenation (HR). Further experiments indicated that baicalin supplementation suppressed the protein expression of RIP1, RIP3 and p-MLKL to interrupt CMEC necroptosis. In addition, baicalin promoted the production of NO via activating the PI3K-AKT-eNOS signaling pathway. Taken together, our results identified the PI3K-AKT-eNOS axis as a new pathway responsible for reperfusion-mediated microvascular damage.
Baicalin protected CMECs in IR rats by promoting the release of NO via the PI3K-AKT-eNOS pathway and mitigated necroptosis by inhibiting the protein expression of RIP1, RIP3 and p-MLKL.
[Display omitted]</description><identifier>ISSN: 0944-7113</identifier><identifier>EISSN: 1618-095X</identifier><identifier>DOI: 10.1016/j.phymed.2019.153035</identifier><identifier>PMID: 31377586</identifier><language>eng</language><publisher>Germany: Elsevier GmbH</publisher><subject>Animals ; Apoptosis - drug effects ; Baicalin ; Cardiac microvascular endothelial cells ; Cardiotonic Agents - pharmacology ; Cell Hypoxia ; Cells, Cultured ; Disease Models, Animal ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - pathology ; ENOS ; Flavonoids - pharmacology ; Ischemia–reperfusion ; Male ; Myocardial Infarction - drug therapy ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocardial Reperfusion Injury - prevention & control ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Necroptosis ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type III - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rats, Wistar ; Signal Transduction - drug effects</subject><ispartof>Phytomedicine (Stuttgart), 2019-10, Vol.63, p.153035-153035, Article 153035</ispartof><rights>2019 Elsevier GmbH</rights><rights>Copyright © 2019 Elsevier GmbH. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-d6b342dcfc676ac12f936d58e8dede111749dfacaf88c188f871645ec4643fb03</citedby><cites>FETCH-LOGICAL-c362t-d6b342dcfc676ac12f936d58e8dede111749dfacaf88c188f871645ec4643fb03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.phymed.2019.153035$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31377586$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bai, Jiannan</creatorcontrib><creatorcontrib>Wang, Qingchao</creatorcontrib><creatorcontrib>Qi, Jiaxin</creatorcontrib><creatorcontrib>Yu, Hongqiang</creatorcontrib><creatorcontrib>Wang, Cong</creatorcontrib><creatorcontrib>Wang, Xiaowei</creatorcontrib><creatorcontrib>Ren, Yanru</creatorcontrib><creatorcontrib>Yang, Fude</creatorcontrib><title>Promoting effect of baicalin on nitric oxide production in CMECs via activating the PI3K-AKT-eNOS pathway attenuates myocardial ischemia–reperfusion injury</title><title>Phytomedicine (Stuttgart)</title><addtitle>Phytomedicine</addtitle><description>Baicalin, which is isolated from Scutellariae Radix, has been shown to possess therapeutic potential for different diseases. Cardiac microvessel injury in myocardial ischemia–reperfusion (IR) has been extensively explored. However, there have been no studies investigating the physiological regulatory mechanisms of baicalin on nitric oxide production and the necroptosis of cardiac microvascular endothelial cells (CMECs) in myocardial IR injury. This study was designed to investigate the contribution of baicalin to repressing necroptosis and preventing IR-mediated CMEC dysfunction.
Indicators of ventricular structure and function were measured by an echocardiographic system. An MTT assay was performed to assess cell viability. Nitrite detection was performed to detect nitric oxide content, and cGMP content was determined using a commercially available cGMP complete ELISA kit. Morphology and molecular characteristics were detected by electron micrographs, quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting.
Our results demonstrated that baicalin significantly improved cardiac function, decreased the myocardial infarction area, and inhibited myocardial cell apoptosis. Moreover, baicalin had a protective effect on cardiac microvessels and promoted the production of nitric oxide (NO) and the level of cGMP in rats that underwent myocardial IR injury. The results of the in vitro experiments showed that baicalin markedly improved cell activity and function in CMECs exposed to hypoxia-reoxygenation (HR). Further experiments indicated that baicalin supplementation suppressed the protein expression of RIP1, RIP3 and p-MLKL to interrupt CMEC necroptosis. In addition, baicalin promoted the production of NO via activating the PI3K-AKT-eNOS signaling pathway. Taken together, our results identified the PI3K-AKT-eNOS axis as a new pathway responsible for reperfusion-mediated microvascular damage.
Baicalin protected CMECs in IR rats by promoting the release of NO via the PI3K-AKT-eNOS pathway and mitigated necroptosis by inhibiting the protein expression of RIP1, RIP3 and p-MLKL.
[Display omitted]</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Baicalin</subject><subject>Cardiac microvascular endothelial cells</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Cell Hypoxia</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - pathology</subject><subject>ENOS</subject><subject>Flavonoids - pharmacology</subject><subject>Ischemia–reperfusion</subject><subject>Male</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Necroptosis</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats, Wistar</subject><subject>Signal Transduction - drug effects</subject><issn>0944-7113</issn><issn>1618-095X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcFu1DAQhi0EokvhDRDykUsWO04c54JUrVqoWmglisTN8tpj1qskDrazkBvvwJmX40nwkvbKaaR__vlnRh9CLylZU0L5m_163M09mHVJaLumNSOsfoRWlFNRkLb-8hitSFtVRUMpO0HPYtwTQqu2IU_RCaOsaWrBV-j3bfC9T274isFa0Al7i7fKadW5AfsBDy4Fp7H_4QzgMXgz6eSynrubD-ebiA9OYZW1g_qXknaAby_ZVXF2dVfAx5tPeFRp913NWKUEw6QSRNzPXqtgnOqwi3oHvVN_fv4KMEKwU1zi91OYn6MnVnURXtzXU_T54vxu8764vnl3uTm7LjTjZSoM37KqNNpq3nClaWlbxk0tQBgwQCltqtZYpZUVQlMhrGgor2rQFa-Y3RJ2il4vufnBbxPEJPt8F3SdGsBPUZYlF3XDWc2ytVqsOvgYA1g5BterMEtK5BGM3MsFjDyCkQuYPPbqfsO0PfYehh5IZMPbxQD5z4ODIKN2MGgwLmQs0nj3_w1_AVXHpRU</recordid><startdate>201910</startdate><enddate>201910</enddate><creator>Bai, Jiannan</creator><creator>Wang, Qingchao</creator><creator>Qi, Jiaxin</creator><creator>Yu, Hongqiang</creator><creator>Wang, Cong</creator><creator>Wang, Xiaowei</creator><creator>Ren, Yanru</creator><creator>Yang, Fude</creator><general>Elsevier GmbH</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201910</creationdate><title>Promoting effect of baicalin on nitric oxide production in CMECs via activating the PI3K-AKT-eNOS pathway attenuates myocardial ischemia–reperfusion injury</title><author>Bai, Jiannan ; Wang, Qingchao ; Qi, Jiaxin ; Yu, Hongqiang ; Wang, Cong ; Wang, Xiaowei ; Ren, Yanru ; Yang, Fude</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-d6b342dcfc676ac12f936d58e8dede111749dfacaf88c188f871645ec4643fb03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Baicalin</topic><topic>Cardiac microvascular endothelial cells</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Cell Hypoxia</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - pathology</topic><topic>ENOS</topic><topic>Flavonoids - pharmacology</topic><topic>Ischemia–reperfusion</topic><topic>Male</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Necroptosis</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats, Wistar</topic><topic>Signal Transduction - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bai, Jiannan</creatorcontrib><creatorcontrib>Wang, Qingchao</creatorcontrib><creatorcontrib>Qi, Jiaxin</creatorcontrib><creatorcontrib>Yu, Hongqiang</creatorcontrib><creatorcontrib>Wang, Cong</creatorcontrib><creatorcontrib>Wang, Xiaowei</creatorcontrib><creatorcontrib>Ren, Yanru</creatorcontrib><creatorcontrib>Yang, Fude</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Phytomedicine (Stuttgart)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bai, Jiannan</au><au>Wang, Qingchao</au><au>Qi, Jiaxin</au><au>Yu, Hongqiang</au><au>Wang, Cong</au><au>Wang, Xiaowei</au><au>Ren, Yanru</au><au>Yang, Fude</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Promoting effect of baicalin on nitric oxide production in CMECs via activating the PI3K-AKT-eNOS pathway attenuates myocardial ischemia–reperfusion injury</atitle><jtitle>Phytomedicine (Stuttgart)</jtitle><addtitle>Phytomedicine</addtitle><date>2019-10</date><risdate>2019</risdate><volume>63</volume><spage>153035</spage><epage>153035</epage><pages>153035-153035</pages><artnum>153035</artnum><issn>0944-7113</issn><eissn>1618-095X</eissn><abstract>Baicalin, which is isolated from Scutellariae Radix, has been shown to possess therapeutic potential for different diseases. Cardiac microvessel injury in myocardial ischemia–reperfusion (IR) has been extensively explored. However, there have been no studies investigating the physiological regulatory mechanisms of baicalin on nitric oxide production and the necroptosis of cardiac microvascular endothelial cells (CMECs) in myocardial IR injury. This study was designed to investigate the contribution of baicalin to repressing necroptosis and preventing IR-mediated CMEC dysfunction.
Indicators of ventricular structure and function were measured by an echocardiographic system. An MTT assay was performed to assess cell viability. Nitrite detection was performed to detect nitric oxide content, and cGMP content was determined using a commercially available cGMP complete ELISA kit. Morphology and molecular characteristics were detected by electron micrographs, quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting.
Our results demonstrated that baicalin significantly improved cardiac function, decreased the myocardial infarction area, and inhibited myocardial cell apoptosis. Moreover, baicalin had a protective effect on cardiac microvessels and promoted the production of nitric oxide (NO) and the level of cGMP in rats that underwent myocardial IR injury. The results of the in vitro experiments showed that baicalin markedly improved cell activity and function in CMECs exposed to hypoxia-reoxygenation (HR). Further experiments indicated that baicalin supplementation suppressed the protein expression of RIP1, RIP3 and p-MLKL to interrupt CMEC necroptosis. In addition, baicalin promoted the production of NO via activating the PI3K-AKT-eNOS signaling pathway. Taken together, our results identified the PI3K-AKT-eNOS axis as a new pathway responsible for reperfusion-mediated microvascular damage.
Baicalin protected CMECs in IR rats by promoting the release of NO via the PI3K-AKT-eNOS pathway and mitigated necroptosis by inhibiting the protein expression of RIP1, RIP3 and p-MLKL.
[Display omitted]</abstract><cop>Germany</cop><pub>Elsevier GmbH</pub><pmid>31377586</pmid><doi>10.1016/j.phymed.2019.153035</doi><tpages>1</tpages></addata></record> |
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| ispartof | Phytomedicine (Stuttgart), 2019-10, Vol.63, p.153035-153035, Article 153035 |
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| subjects | Animals Apoptosis - drug effects Baicalin Cardiac microvascular endothelial cells Cardiotonic Agents - pharmacology Cell Hypoxia Cells, Cultured Disease Models, Animal Endothelial Cells - drug effects Endothelial Cells - metabolism Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - pathology ENOS Flavonoids - pharmacology Ischemia–reperfusion Male Myocardial Infarction - drug therapy Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - prevention & control Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Necroptosis Nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase Type III - metabolism Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Rats, Wistar Signal Transduction - drug effects |
| title | Promoting effect of baicalin on nitric oxide production in CMECs via activating the PI3K-AKT-eNOS pathway attenuates myocardial ischemia–reperfusion injury |
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