Ginsenoside Rg-1 prevents elevated cytosolic Ca2+ via store-operated Ca2+ entry in high-glucose–stimulated vascular endothelial and smooth muscle cells
Abstract Background Ginsenoside Rg-1 (Rg-1), a triterpenoid saponin abundantly present in Panax ginseng, is a type of naturally occurring steroid with known anti-diabetic and anti-inflammatory effects. In this study, we sought to confirm the effects and mechanisms of action of Rg-1 on store-operated...
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BMC
2022-06-01
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Series: | BMC Complementary Medicine and Therapies |
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Online Access: | https://doi.org/10.1186/s12906-022-03647-5 |
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author | A Young Han Su Min Ha You Kyoung Shin Geun Hee Seol |
author_facet | A Young Han Su Min Ha You Kyoung Shin Geun Hee Seol |
author_sort | A Young Han |
collection | DOAJ |
description | Abstract Background Ginsenoside Rg-1 (Rg-1), a triterpenoid saponin abundantly present in Panax ginseng, is a type of naturally occurring steroid with known anti-diabetic and anti-inflammatory effects. In this study, we sought to confirm the effects and mechanisms of action of Rg-1 on store-operated Ca2+ entry (SOCE) in human vascular endothelial cell line (EA) and murine aortic vascular smooth muscle cell line (MOVAS) cells exposed to high glucose. Methods Cytosolic Ca2+ concentrations in EA and MOVAS cells were measured by monitoring fluorescence of the ratiometric Ca2+-indicator, Fura-2 AM. Results High glucose significantly increased Ca2+ influx by abnormally activating SOCE in EA and MOVAS cells. Notably, this high glucose-induced increase in SOCE was restored to normal levels in EA and MOVAS cells by Rg-1. Moreover, Rg-1 induced reductions in SOCE in cells exposed to high glucose were significantly inhibited by the plasma membrane Ca2+ ATPase (PMCA) blocker lanthanum, the Na+/K+-ATPase blocker ouabain, or the Na+/Ca2+ exchanger (NCX) blockers Ni2+ and KB-R7943. These observations suggest that the mechanism of action of Rg-1 inhibition of SOCE involves PMCA and Na+/K+-ATPase, and an increase in Ca2+ efflux via NCXs in both EA and MOVAS cells exposed to high glucose. Conclusions These findings indicate that Rg-1 may protect vascular endothelial and smooth muscle cells from Ca2+ increases following exposure to hyperglycemic conditions. |
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language | English |
last_indexed | 2024-04-13T16:59:26Z |
publishDate | 2022-06-01 |
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series | BMC Complementary Medicine and Therapies |
spelling | doaj.art-51b591acfc8e43d48287ad8aac7c0c8b2022-12-22T02:38:43ZengBMCBMC Complementary Medicine and Therapies2662-76712022-06-0122111010.1186/s12906-022-03647-5Ginsenoside Rg-1 prevents elevated cytosolic Ca2+ via store-operated Ca2+ entry in high-glucose–stimulated vascular endothelial and smooth muscle cellsA Young Han0Su Min Ha1You Kyoung Shin2Geun Hee Seol3Department of Basic Nursing Science, College of Nursing, Korea UniversityDepartment of Basic Nursing Science, College of Nursing, Korea UniversityDepartment of Basic Nursing Science, College of Nursing, Korea UniversityDepartment of Basic Nursing Science, College of Nursing, Korea UniversityAbstract Background Ginsenoside Rg-1 (Rg-1), a triterpenoid saponin abundantly present in Panax ginseng, is a type of naturally occurring steroid with known anti-diabetic and anti-inflammatory effects. In this study, we sought to confirm the effects and mechanisms of action of Rg-1 on store-operated Ca2+ entry (SOCE) in human vascular endothelial cell line (EA) and murine aortic vascular smooth muscle cell line (MOVAS) cells exposed to high glucose. Methods Cytosolic Ca2+ concentrations in EA and MOVAS cells were measured by monitoring fluorescence of the ratiometric Ca2+-indicator, Fura-2 AM. Results High glucose significantly increased Ca2+ influx by abnormally activating SOCE in EA and MOVAS cells. Notably, this high glucose-induced increase in SOCE was restored to normal levels in EA and MOVAS cells by Rg-1. Moreover, Rg-1 induced reductions in SOCE in cells exposed to high glucose were significantly inhibited by the plasma membrane Ca2+ ATPase (PMCA) blocker lanthanum, the Na+/K+-ATPase blocker ouabain, or the Na+/Ca2+ exchanger (NCX) blockers Ni2+ and KB-R7943. These observations suggest that the mechanism of action of Rg-1 inhibition of SOCE involves PMCA and Na+/K+-ATPase, and an increase in Ca2+ efflux via NCXs in both EA and MOVAS cells exposed to high glucose. Conclusions These findings indicate that Rg-1 may protect vascular endothelial and smooth muscle cells from Ca2+ increases following exposure to hyperglycemic conditions.https://doi.org/10.1186/s12906-022-03647-5Ginsenoside Rg-1Store-operated Ca2+ entryHigh glucoseVascular endothelial cellsVascular smooth muscle cells |
spellingShingle | A Young Han Su Min Ha You Kyoung Shin Geun Hee Seol Ginsenoside Rg-1 prevents elevated cytosolic Ca2+ via store-operated Ca2+ entry in high-glucose–stimulated vascular endothelial and smooth muscle cells BMC Complementary Medicine and Therapies Ginsenoside Rg-1 Store-operated Ca2+ entry High glucose Vascular endothelial cells Vascular smooth muscle cells |
title | Ginsenoside Rg-1 prevents elevated cytosolic Ca2+ via store-operated Ca2+ entry in high-glucose–stimulated vascular endothelial and smooth muscle cells |
title_full | Ginsenoside Rg-1 prevents elevated cytosolic Ca2+ via store-operated Ca2+ entry in high-glucose–stimulated vascular endothelial and smooth muscle cells |
title_fullStr | Ginsenoside Rg-1 prevents elevated cytosolic Ca2+ via store-operated Ca2+ entry in high-glucose–stimulated vascular endothelial and smooth muscle cells |
title_full_unstemmed | Ginsenoside Rg-1 prevents elevated cytosolic Ca2+ via store-operated Ca2+ entry in high-glucose–stimulated vascular endothelial and smooth muscle cells |
title_short | Ginsenoside Rg-1 prevents elevated cytosolic Ca2+ via store-operated Ca2+ entry in high-glucose–stimulated vascular endothelial and smooth muscle cells |
title_sort | ginsenoside rg 1 prevents elevated cytosolic ca2 via store operated ca2 entry in high glucose stimulated vascular endothelial and smooth muscle cells |
topic | Ginsenoside Rg-1 Store-operated Ca2+ entry High glucose Vascular endothelial cells Vascular smooth muscle cells |
url | https://doi.org/10.1186/s12906-022-03647-5 |
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