Ginsenoside Rg-1 prevents elevated cytosolic Ca2+ via store-operated Ca2+ entry in high-glucose-stimulated vascular endothelial and smooth muscle cellsopen access
- Authors
- Han, A. Young; Ha, Su Min; Shin, You Kyoung; Seol, Geun Hee
- Issue Date
- 22-6월-2022
- Publisher
- BMC
- Keywords
- Ginsenoside Rg-1; Store-operated Ca2+ entry; High glucose; Vascular endothelial cells; Vascular smooth muscle cells
- Citation
- BMC COMPLEMENTARY MEDICINE AND THERAPIES, v.22, no.1
- Indexed
- SCIE
SCOPUS
- Journal Title
- BMC COMPLEMENTARY MEDICINE AND THERAPIES
- Volume
- 22
- Number
- 1
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/142791
- DOI
- 10.1186/s12906-022-03647-5
- ISSN
- 2662-7671
- 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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