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
Hauptverfasser: Ma, Yu-Guang, Wang, Jun-Wei, Zhang, Yin-Bin, Wang, Bao-Feng, Dai, Zhi-Jun, Xie, Man-Jiang, Kang, Hua-Feng
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container_issue 3
container_start_page 365
container_title Cell and tissue research
container_volume 370
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
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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><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). 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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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source SpringerNature Journals
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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