Salidroside improved cerebrovascular vasodilation in streptozotocin-induced diabetic rats through restoring the function of BKCa channel in smooth muscle cells
Vessel disease is a kind of severe complication in diabetic patients. However, few pharmacologic agents can directly recover diabetic vascular function. Salidroside (SAL), a major ingredient from Rhodiola rosea , has been found to have an obvious hypoglycemic effect and a beneficial protection on va...
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Veröffentlicht in: | Cell and tissue research 2017-12, Vol.370 (3), p.365-377 |
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creator | Ma, Yu-Guang Wang, Jun-Wei Zhang, Yin-Bin Wang, Bao-Feng Dai, Zhi-Jun Xie, Man-Jiang Kang, Hua-Feng |
description | Vessel disease is a kind of severe complication in diabetic patients. However, few pharmacologic agents can directly recover diabetic vascular function. Salidroside (SAL), a major ingredient from
Rhodiola rosea
, has been found to have an obvious hypoglycemic effect and a beneficial protection on vascular function in diabetes. However, whether SAL is a suitable treatment for diabetes has not so far been evaluated and the underlying mechanisms remain unknown. The present work aims to (1) investigate the potential effects of SAL on cerebrovascular relaxation in streptozotocin-induced diabetic rats or when exposed to acute hyperglycemia condition and (2) examine whether function of the BK
Ca
channel is involved in SAL treatment for diabetic vascular relaxation. Our results indicate that chronic administration of 100 mg/kg/day SAL not only improves cerebrovascular relaxation but also increases BK
Ca
β1-subunit expressions at both protein and mRNA levels and enhances BK
Ca
whole-cell and single-channel activities in cerebral VSMCs of diabetic rats. Correspondingly, acute application of 100 μM SAL induces cerebrovascular relaxation by activation of the BK
Ca
channel. Furthermore, SAL activated the BK
Ca
channel mainly through acting on the β1-subunit in HEK293 cells transfected with
hSlo
α+β1 constructs. We concluded that SAL improved vasodilation in diabetic rats through restoring the function of the BK
Ca
-β1 subunit in cerebrovascular smooth muscle cells, which may be the underlying mechanism responsible for the vascular protection of SAL in diabetes. |
doi_str_mv | 10.1007/s00441-017-2671-3 |
format | Article |
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Rhodiola rosea
, has been found to have an obvious hypoglycemic effect and a beneficial protection on vascular function in diabetes. However, whether SAL is a suitable treatment for diabetes has not so far been evaluated and the underlying mechanisms remain unknown. The present work aims to (1) investigate the potential effects of SAL on cerebrovascular relaxation in streptozotocin-induced diabetic rats or when exposed to acute hyperglycemia condition and (2) examine whether function of the BK
Ca
channel is involved in SAL treatment for diabetic vascular relaxation. Our results indicate that chronic administration of 100 mg/kg/day SAL not only improves cerebrovascular relaxation but also increases BK
Ca
β1-subunit expressions at both protein and mRNA levels and enhances BK
Ca
whole-cell and single-channel activities in cerebral VSMCs of diabetic rats. Correspondingly, acute application of 100 μM SAL induces cerebrovascular relaxation by activation of the BK
Ca
channel. Furthermore, SAL activated the BK
Ca
channel mainly through acting on the β1-subunit in HEK293 cells transfected with
hSlo
α+β1 constructs. We concluded that SAL improved vasodilation in diabetic rats through restoring the function of the BK
Ca
-β1 subunit in cerebrovascular smooth muscle cells, which may be the underlying mechanism responsible for the vascular protection of SAL in diabetes.</description><identifier>ISSN: 0302-766X</identifier><identifier>EISSN: 1432-0878</identifier><identifier>DOI: 10.1007/s00441-017-2671-3</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Biomedical and Life Sciences ; Biomedicine ; Cerebrovascular system ; Diabetes ; Diabetes mellitus ; Human Genetics ; Hyperglycemia ; Molecular Medicine ; mRNA ; Muscles ; Proteomics ; Rats ; Regular Article ; Rodents ; Smooth muscle ; Streptozocin ; Vasodilation</subject><ispartof>Cell and tissue research, 2017-12, Vol.370 (3), p.365-377</ispartof><rights>Springer-Verlag GmbH Germany 2017</rights><rights>Cell and Tissue Research is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c349t-425fa9b100803d026e72ca01a2771c1d7acc83b610db22b0d585401f96e4f0bb3</citedby><cites>FETCH-LOGICAL-c349t-425fa9b100803d026e72ca01a2771c1d7acc83b610db22b0d585401f96e4f0bb3</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/s00441-017-2671-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00441-017-2671-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids></links><search><creatorcontrib>Ma, Yu-Guang</creatorcontrib><creatorcontrib>Wang, Jun-Wei</creatorcontrib><creatorcontrib>Zhang, Yin-Bin</creatorcontrib><creatorcontrib>Wang, Bao-Feng</creatorcontrib><creatorcontrib>Dai, Zhi-Jun</creatorcontrib><creatorcontrib>Xie, Man-Jiang</creatorcontrib><creatorcontrib>Kang, Hua-Feng</creatorcontrib><title>Salidroside improved cerebrovascular vasodilation in streptozotocin-induced diabetic rats through restoring the function of BKCa channel in smooth muscle cells</title><title>Cell and tissue research</title><addtitle>Cell Tissue Res</addtitle><description>Vessel disease is a kind of severe complication in diabetic patients. However, few pharmacologic agents can directly recover diabetic vascular function. Salidroside (SAL), a major ingredient from
Rhodiola rosea
, has been found to have an obvious hypoglycemic effect and a beneficial protection on vascular function in diabetes. However, whether SAL is a suitable treatment for diabetes has not so far been evaluated and the underlying mechanisms remain unknown. The present work aims to (1) investigate the potential effects of SAL on cerebrovascular relaxation in streptozotocin-induced diabetic rats or when exposed to acute hyperglycemia condition and (2) examine whether function of the BK
Ca
channel is involved in SAL treatment for diabetic vascular relaxation. Our results indicate that chronic administration of 100 mg/kg/day SAL not only improves cerebrovascular relaxation but also increases BK
Ca
β1-subunit expressions at both protein and mRNA levels and enhances BK
Ca
whole-cell and single-channel activities in cerebral VSMCs of diabetic rats. Correspondingly, acute application of 100 μM SAL induces cerebrovascular relaxation by activation of the BK
Ca
channel. Furthermore, SAL activated the BK
Ca
channel mainly through acting on the β1-subunit in HEK293 cells transfected with
hSlo
α+β1 constructs. We concluded that SAL improved vasodilation in diabetic rats through restoring the function of the BK
Ca
-β1 subunit in cerebrovascular smooth muscle cells, which may be the underlying mechanism responsible for the vascular protection of SAL in diabetes.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cerebrovascular system</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Human Genetics</subject><subject>Hyperglycemia</subject><subject>Molecular Medicine</subject><subject>mRNA</subject><subject>Muscles</subject><subject>Proteomics</subject><subject>Rats</subject><subject>Regular Article</subject><subject>Rodents</subject><subject>Smooth muscle</subject><subject>Streptozocin</subject><subject>Vasodilation</subject><issn>0302-766X</issn><issn>1432-0878</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kc9qFTEYxYMoeFt9AHeBbtyk_fLnJjPLemmrtOBCBXchk2R6U2aS2yQj6Mv4qmZ6uxDBVT7COT8O5yD0jsI5BVAXBUAISoAqwqSihL9AGyo4I9Cp7iXaAAdGlJTfX6OTUh4AqJCy36DfX8wUXE4lOI_DfMjph3fY-uyHdppil8lk3I7kwmRqSBGHiEvN_lDTr1STDZGE6BbbbC6YwddgcTa14LrPabnf4-xLTTnE-_bj8bhE-4RJI_5wuzPY7k2MfnrCzinVPZ6XYiffQkxTeYNejWYq_u3ze4q-XV993X0kd59vPu0u74jloq9EsO1o-qFV0QF3wKRXzBqghilFLXXKWNvxQVJwA2MDuG23FUDHXnoxwjDwU_T-yG0NPC4tsZ5DWROY6NNSNO1ZK5Irzpv07B_pQ1pybOmaSna9oLAVTUWPKtvKLdmP-pDDbPJPTUGvk-njZLpNptfJ9EpmR085rH35_Bf5v6Y_C_Kc5A</recordid><startdate>20171201</startdate><enddate>20171201</enddate><creator>Ma, Yu-Guang</creator><creator>Wang, Jun-Wei</creator><creator>Zhang, Yin-Bin</creator><creator>Wang, Bao-Feng</creator><creator>Dai, Zhi-Jun</creator><creator>Xie, Man-Jiang</creator><creator>Kang, Hua-Feng</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7RV</scope><scope>7SS</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20171201</creationdate><title>Salidroside improved cerebrovascular vasodilation in streptozotocin-induced diabetic rats through restoring the function of BKCa channel in smooth muscle cells</title><author>Ma, Yu-Guang ; Wang, Jun-Wei ; Zhang, Yin-Bin ; Wang, Bao-Feng ; Dai, Zhi-Jun ; Xie, Man-Jiang ; Kang, Hua-Feng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c349t-425fa9b100803d026e72ca01a2771c1d7acc83b610db22b0d585401f96e4f0bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cerebrovascular system</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Human Genetics</topic><topic>Hyperglycemia</topic><topic>Molecular Medicine</topic><topic>mRNA</topic><topic>Muscles</topic><topic>Proteomics</topic><topic>Rats</topic><topic>Regular Article</topic><topic>Rodents</topic><topic>Smooth muscle</topic><topic>Streptozocin</topic><topic>Vasodilation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Yu-Guang</creatorcontrib><creatorcontrib>Wang, Jun-Wei</creatorcontrib><creatorcontrib>Zhang, Yin-Bin</creatorcontrib><creatorcontrib>Wang, Bao-Feng</creatorcontrib><creatorcontrib>Dai, Zhi-Jun</creatorcontrib><creatorcontrib>Xie, Man-Jiang</creatorcontrib><creatorcontrib>Kang, Hua-Feng</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell and tissue research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Yu-Guang</au><au>Wang, Jun-Wei</au><au>Zhang, Yin-Bin</au><au>Wang, Bao-Feng</au><au>Dai, Zhi-Jun</au><au>Xie, Man-Jiang</au><au>Kang, Hua-Feng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Salidroside improved cerebrovascular vasodilation in streptozotocin-induced diabetic rats through restoring the function of BKCa channel in smooth muscle cells</atitle><jtitle>Cell and tissue research</jtitle><stitle>Cell Tissue Res</stitle><date>2017-12-01</date><risdate>2017</risdate><volume>370</volume><issue>3</issue><spage>365</spage><epage>377</epage><pages>365-377</pages><issn>0302-766X</issn><eissn>1432-0878</eissn><abstract>Vessel disease is a kind of severe complication in diabetic patients. However, few pharmacologic agents can directly recover diabetic vascular function. Salidroside (SAL), a major ingredient from
Rhodiola rosea
, has been found to have an obvious hypoglycemic effect and a beneficial protection on vascular function in diabetes. However, whether SAL is a suitable treatment for diabetes has not so far been evaluated and the underlying mechanisms remain unknown. The present work aims to (1) investigate the potential effects of SAL on cerebrovascular relaxation in streptozotocin-induced diabetic rats or when exposed to acute hyperglycemia condition and (2) examine whether function of the BK
Ca
channel is involved in SAL treatment for diabetic vascular relaxation. Our results indicate that chronic administration of 100 mg/kg/day SAL not only improves cerebrovascular relaxation but also increases BK
Ca
β1-subunit expressions at both protein and mRNA levels and enhances BK
Ca
whole-cell and single-channel activities in cerebral VSMCs of diabetic rats. Correspondingly, acute application of 100 μM SAL induces cerebrovascular relaxation by activation of the BK
Ca
channel. Furthermore, SAL activated the BK
Ca
channel mainly through acting on the β1-subunit in HEK293 cells transfected with
hSlo
α+β1 constructs. We concluded that SAL improved vasodilation in diabetic rats through restoring the function of the BK
Ca
-β1 subunit in cerebrovascular smooth muscle cells, which may be the underlying mechanism responsible for the vascular protection of SAL in diabetes.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><doi>10.1007/s00441-017-2671-3</doi><tpages>13</tpages></addata></record> |
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subjects | Biomedical and Life Sciences Biomedicine Cerebrovascular system Diabetes Diabetes mellitus Human Genetics Hyperglycemia Molecular Medicine mRNA Muscles Proteomics Rats Regular Article Rodents Smooth muscle Streptozocin Vasodilation |
title | Salidroside improved cerebrovascular vasodilation in streptozotocin-induced diabetic rats through restoring the function of BKCa channel in smooth muscle cells |
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