Tanshinone IIA ameliorated endothelial dysfunction in rats with chronic intermittent hypoxia
Chronic intermittent hypoxia (CIH) during repetitive airflow cessations may cause endothelial dysfunction. Tanshinone IIA (Tan IIA) has been used to treat various circulatory disturbance-related diseases because of its pharmacological actions, including vasodilation. However, the mechanism of the ef...
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| Veröffentlicht in: | Cardiovascular pathology 2017-11, Vol.31, p.47-53 |
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| creator | Chen, Lingling Guo, Qiu-Hong Chang, Yue Zhao, Ya-Shuo Li, Ai-Ying Ji, En-Sheng |
| description | Chronic intermittent hypoxia (CIH) during repetitive airflow cessations may cause endothelial dysfunction. Tanshinone IIA (Tan IIA) has been used to treat various circulatory disturbance-related diseases because of its pharmacological actions, including vasodilation. However, the mechanism of the effect of its vasodilation is not well established. The objective of this study was to explore the effect of Tan IIA in endothelium-dependent contracting factors and endothelin receptors in aortic endothelial dysfunction in CIH rats. Aortas of rats were retrieved for use in in vitro experiments (isometric force measurement), histological analysis, immunohistochemistry, and Western blotting. Tan IIA treatment increased the expression of endothelial nitric oxide synthase (eNOS) and formation of nitric oxide (NO), inhibited the production of endothelin-1 (ET-1), down-regulated ETA receptor expression, and up-regulated ETB receptor expression. In conclusion, Tan IIA protects endothelial function by inhibiting strain-induced ET-1 expression, decreasing ETA receptors, increasing ETB receptors, increasing the formation of NO, and up-regulating eNOS in CIH.
•Tan IIA treatment of rats exposed to CIH improved the ACh-induced endothelium-dependent vasorelaxation.•Tan IIA treatment of rats exposed to CIH increased eNOS expression and NO formation in the aortic tissue.•Tan IIA treatment of rats exposed to CIH decreased aortic tissue ET-1 production.•Tan IIA treatment of rats exposed to CIH decreased ETA and increased ETB receptor expression in the aortic tissue. |
| doi_str_mv | 10.1016/j.carpath.2017.06.008 |
| format | Article |
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•Tan IIA treatment of rats exposed to CIH improved the ACh-induced endothelium-dependent vasorelaxation.•Tan IIA treatment of rats exposed to CIH increased eNOS expression and NO formation in the aortic tissue.•Tan IIA treatment of rats exposed to CIH decreased aortic tissue ET-1 production.•Tan IIA treatment of rats exposed to CIH decreased ETA and increased ETB receptor expression in the aortic tissue.</description><identifier>ISSN: 1054-8807</identifier><identifier>EISSN: 1879-1336</identifier><identifier>DOI: 10.1016/j.carpath.2017.06.008</identifier><identifier>PMID: 28985491</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Chronic intermittent hypoxia ; Diterpenes, Abietane - pharmacology ; Endothelial dysfunction ; Endothelin-1 - drug effects ; Endothelin-1 - metabolism ; Endothelium, Vascular - drug effects ; Hypoxia - metabolism ; Nitric Oxide - biosynthesis ; Nitric Oxide Synthase Type III - biosynthesis ; Rats ; Receptors, Endothelin - drug effects ; Receptors, Endothelin - metabolism ; Sleep Apnea, Obstructive - metabolism ; Tanshinone IIA ; Vasodilator Agents - pharmacology</subject><ispartof>Cardiovascular pathology, 2017-11, Vol.31, p.47-53</ispartof><rights>2017 Elsevier Inc.</rights><rights>Copyright © 2017 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c365t-da64efcd06b7dc0bb21d6cd31109c31bbd3b3a95f111ef5a35ae8ae00484a5123</citedby><cites>FETCH-LOGICAL-c365t-da64efcd06b7dc0bb21d6cd31109c31bbd3b3a95f111ef5a35ae8ae00484a5123</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.carpath.2017.06.008$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27907,27908,45978</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28985491$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Lingling</creatorcontrib><creatorcontrib>Guo, Qiu-Hong</creatorcontrib><creatorcontrib>Chang, Yue</creatorcontrib><creatorcontrib>Zhao, Ya-Shuo</creatorcontrib><creatorcontrib>Li, Ai-Ying</creatorcontrib><creatorcontrib>Ji, En-Sheng</creatorcontrib><title>Tanshinone IIA ameliorated endothelial dysfunction in rats with chronic intermittent hypoxia</title><title>Cardiovascular pathology</title><addtitle>Cardiovasc Pathol</addtitle><description>Chronic intermittent hypoxia (CIH) during repetitive airflow cessations may cause endothelial dysfunction. Tanshinone IIA (Tan IIA) has been used to treat various circulatory disturbance-related diseases because of its pharmacological actions, including vasodilation. However, the mechanism of the effect of its vasodilation is not well established. The objective of this study was to explore the effect of Tan IIA in endothelium-dependent contracting factors and endothelin receptors in aortic endothelial dysfunction in CIH rats. Aortas of rats were retrieved for use in in vitro experiments (isometric force measurement), histological analysis, immunohistochemistry, and Western blotting. Tan IIA treatment increased the expression of endothelial nitric oxide synthase (eNOS) and formation of nitric oxide (NO), inhibited the production of endothelin-1 (ET-1), down-regulated ETA receptor expression, and up-regulated ETB receptor expression. In conclusion, Tan IIA protects endothelial function by inhibiting strain-induced ET-1 expression, decreasing ETA receptors, increasing ETB receptors, increasing the formation of NO, and up-regulating eNOS in CIH.
•Tan IIA treatment of rats exposed to CIH improved the ACh-induced endothelium-dependent vasorelaxation.•Tan IIA treatment of rats exposed to CIH increased eNOS expression and NO formation in the aortic tissue.•Tan IIA treatment of rats exposed to CIH decreased aortic tissue ET-1 production.•Tan IIA treatment of rats exposed to CIH decreased ETA and increased ETB receptor expression in the aortic tissue.</description><subject>Animals</subject><subject>Chronic intermittent hypoxia</subject><subject>Diterpenes, Abietane - pharmacology</subject><subject>Endothelial dysfunction</subject><subject>Endothelin-1 - drug effects</subject><subject>Endothelin-1 - metabolism</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Hypoxia - metabolism</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide Synthase Type III - biosynthesis</subject><subject>Rats</subject><subject>Receptors, Endothelin - drug effects</subject><subject>Receptors, Endothelin - metabolism</subject><subject>Sleep Apnea, Obstructive - metabolism</subject><subject>Tanshinone IIA</subject><subject>Vasodilator Agents - pharmacology</subject><issn>1054-8807</issn><issn>1879-1336</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1P3DAQQC0EKrDtT6DykUuCHTuOc0II0bISEhe4VbIce6J4ldhb20vZf1-j3fbKaT70ZkbzELqipKaEiptNbXTc6jzVDaFdTURNiDxBF1R2fUUZE6clJy2vpCTdObpMaUMKwTn_gs4b2cuW9_QC_XrRPk3OBw94vb7DeoHZhagzWAzehjyVWs_Y7tO48ya74LHzuAAJ_3F5wmaKwTtTmhni4nIGn_G034Z3p7-is1HPCb4d4wq9_nh4uX-snp5_ru_vnirDRJsrqwWH0Vgihs4aMgwNtcJYRinpDaPDYNnAdN-OlFIYW81aDVIDIVxy3dKGrdD1Ye82ht87SFktLhmYZ-0h7JKiPZedaHjRskLtATUxpBRhVNvoFh33ihL1IVZt1FGs-hCriFBFW5n7fjyxGxaw_6f-mSzA7QGA8uibg6iSceANWBfBZGWD--TEX6qsjrA</recordid><startdate>201711</startdate><enddate>201711</enddate><creator>Chen, Lingling</creator><creator>Guo, Qiu-Hong</creator><creator>Chang, Yue</creator><creator>Zhao, Ya-Shuo</creator><creator>Li, Ai-Ying</creator><creator>Ji, En-Sheng</creator><general>Elsevier Inc</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>201711</creationdate><title>Tanshinone IIA ameliorated endothelial dysfunction in rats with chronic intermittent hypoxia</title><author>Chen, Lingling ; Guo, Qiu-Hong ; Chang, Yue ; Zhao, Ya-Shuo ; Li, Ai-Ying ; Ji, En-Sheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c365t-da64efcd06b7dc0bb21d6cd31109c31bbd3b3a95f111ef5a35ae8ae00484a5123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Chronic intermittent hypoxia</topic><topic>Diterpenes, Abietane - pharmacology</topic><topic>Endothelial dysfunction</topic><topic>Endothelin-1 - drug effects</topic><topic>Endothelin-1 - metabolism</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Hypoxia - metabolism</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide Synthase Type III - biosynthesis</topic><topic>Rats</topic><topic>Receptors, Endothelin - drug effects</topic><topic>Receptors, Endothelin - metabolism</topic><topic>Sleep Apnea, Obstructive - metabolism</topic><topic>Tanshinone IIA</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Lingling</creatorcontrib><creatorcontrib>Guo, Qiu-Hong</creatorcontrib><creatorcontrib>Chang, Yue</creatorcontrib><creatorcontrib>Zhao, Ya-Shuo</creatorcontrib><creatorcontrib>Li, Ai-Ying</creatorcontrib><creatorcontrib>Ji, En-Sheng</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>Cardiovascular pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Lingling</au><au>Guo, Qiu-Hong</au><au>Chang, Yue</au><au>Zhao, Ya-Shuo</au><au>Li, Ai-Ying</au><au>Ji, En-Sheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tanshinone IIA ameliorated endothelial dysfunction in rats with chronic intermittent hypoxia</atitle><jtitle>Cardiovascular pathology</jtitle><addtitle>Cardiovasc Pathol</addtitle><date>2017-11</date><risdate>2017</risdate><volume>31</volume><spage>47</spage><epage>53</epage><pages>47-53</pages><issn>1054-8807</issn><eissn>1879-1336</eissn><abstract>Chronic intermittent hypoxia (CIH) during repetitive airflow cessations may cause endothelial dysfunction. Tanshinone IIA (Tan IIA) has been used to treat various circulatory disturbance-related diseases because of its pharmacological actions, including vasodilation. However, the mechanism of the effect of its vasodilation is not well established. The objective of this study was to explore the effect of Tan IIA in endothelium-dependent contracting factors and endothelin receptors in aortic endothelial dysfunction in CIH rats. Aortas of rats were retrieved for use in in vitro experiments (isometric force measurement), histological analysis, immunohistochemistry, and Western blotting. Tan IIA treatment increased the expression of endothelial nitric oxide synthase (eNOS) and formation of nitric oxide (NO), inhibited the production of endothelin-1 (ET-1), down-regulated ETA receptor expression, and up-regulated ETB receptor expression. In conclusion, Tan IIA protects endothelial function by inhibiting strain-induced ET-1 expression, decreasing ETA receptors, increasing ETB receptors, increasing the formation of NO, and up-regulating eNOS in CIH.
•Tan IIA treatment of rats exposed to CIH improved the ACh-induced endothelium-dependent vasorelaxation.•Tan IIA treatment of rats exposed to CIH increased eNOS expression and NO formation in the aortic tissue.•Tan IIA treatment of rats exposed to CIH decreased aortic tissue ET-1 production.•Tan IIA treatment of rats exposed to CIH decreased ETA and increased ETB receptor expression in the aortic tissue.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>28985491</pmid><doi>10.1016/j.carpath.2017.06.008</doi><tpages>7</tpages></addata></record> |
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| subjects | Animals Chronic intermittent hypoxia Diterpenes, Abietane - pharmacology Endothelial dysfunction Endothelin-1 - drug effects Endothelin-1 - metabolism Endothelium, Vascular - drug effects Hypoxia - metabolism Nitric Oxide - biosynthesis Nitric Oxide Synthase Type III - biosynthesis Rats Receptors, Endothelin - drug effects Receptors, Endothelin - metabolism Sleep Apnea, Obstructive - metabolism Tanshinone IIA Vasodilator Agents - pharmacology |
| title | Tanshinone IIA ameliorated endothelial dysfunction in rats with chronic intermittent hypoxia |
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