Salvianolic acid B protects against oxLDL-induced endothelial dysfunction under high-glucose conditions by downregulating ROCK1-mediated mitophagy and apoptosis
- Authors
- Ko, Young Shin; Jin, Hana; Park, Sang Won; Kim, Hye Jung
- Issue Date
- Apr-2020
- Publisher
- Elsevier BV
- Keywords
- Apoptosis; Endothelial cells; High glucose; Mitophagy; oxLDL; Salvianolic acid B
- Citation
- Biochemical Pharmacology, v.174
- Indexed
- SCIE
SCOPUS
- Journal Title
- Biochemical Pharmacology
- Volume
- 174
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/6785
- DOI
- 10.1016/j.bcp.2020.113815
- ISSN
- 0006-2952
1873-2968
- Abstract
- Diabetes is related to alterations in glucose and lipid metabolism, which are linked to endothelial cell (EC) dysfunction. Salvianolic acid B (Sal B), one of the major ingredient of Danshen (Salvia miltiorrhiza), possesses many of the biological activities. However, protective effect of Sal B against oxLDL induced ECs dysfunction under high glucose condition (high Glu) is not well known. Thus, in this study, we investigated the protective effects of Sal B against EC dysfunction induced by oxLDL and high Glu and examined the associated mechanisms. Our results showed that Sal B significantly and dose-dependently decreased oxLDL- and high Glu-mediated induction of lectin-like oxLDL receptor-1 and significantly decreased oxLDL- and high Glu-induced mitochondrial ROS (mtROS) production and mitochondrial DNA (mtDNA) expression. In addition, oxLDL stimulation under high-Glu conditions activated the intrinsic apoptosis pathway in ECs. These effects were abolished by Sal B through reductions in mtROS and mtDNA. Furthermore, Sal B inhibited oxLDL- and high Glu-induced increases in fission protein (p-DRP 1 and FIS 1) levels. OxLDL and high Glu activated the ROCK1 pathway, which is involved in apoptosis and mitophagy, while Sal B significantly reduced ROCK1 protein levels. The protective effects of Sal B against oxLDL- and high Glu-induced endothelial dysfunction may be mediated by reductions in apoptosis-related proteins and fission proteins through suppression of the ROCK1-mediated pathway.
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