Salvianolic Acid B Inhibits Atherogenesis of Vascular Cells through Induction of Nrf2-dependent Heme Oxygenase-1

ISSN: 1875-533X (Online)
ISSN: 0929-8673 (Print)

Volume 24, 42 Issues, 2017

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Current Medicinal Chemistry

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Atta-ur-Rahman, FRS
Honorary Life Fellow
Kings College
University of Cambridge

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Salvianolic Acid B Inhibits Atherogenesis of Vascular Cells through Induction of Nrf2-dependent Heme Oxygenase-1

Current Medicinal Chemistry, 21(26): 3095-3106.

Author(s): Hyun Jung Lee, MiRanSeo and Eun Jig Lee.

Affiliation: Severance Integrative Research Institute for Cerebral & Cardiovascular Disease, Yonsei University College of Medicine, 50Yonsei-ro, Seodaemun-gu, Seoul120-752, Korea.


Aims: Salvianolic acid B (Sal B), one of the most active components of Danshen extracts, has beneficial roles in the prevention and treatment of cardiovascular diseases. However, the precise mechanism by which Sal B exerts its effects on vascular cells is unclear. We aimed to elucidate the effects of Sal B on vascular cells and the underlying mechanisms. Methods and Results: Treatment of vascular smooth muscle cells with Sal B effectively inhibited platelet-derived growth factor (PDGF)-induced cell proliferation and migration, and markedly increased heme oxygenase-1 (HO-1) expression. These changes were accompanied by antioxidant effects, including decreases in the generation of reactive oxygen species and the NADP/NADPH ratio. In human umbilical vein endothelial cells, Sal B also strongly induced HO-1 and effectively inhibited tumor necrosis factor- α-induced NF- κB activation. Knockdown of HO-1 expression by siRNA abolished the effects of Sal B in vascular cells and prevented the inhibition of proliferation, migration, and inflammation in HO-1-deficient cells. In ex vivo culture of arterial rings isolated from nuclear factor-E2-related factor 2 (Nrf2)-knockout mice, Sal B neither induce HO-1 expression and nor inhibit PDGF-induced neointimal hyperplasia in arteries, suggesting that Nrf2 plays a crucial role in the induction of HO-1 expression. Conclusions: We conclude that Sal B exerts antiatherogenic effects by inhibiting the proliferation, migration, and inflammation of vascular cells through induction of HO-1 via Nrf2 activation.


HO-1, HUVEC, inflammation, Nrf2, proliferation, Salvianolic acid B, VSMC.

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Article Details

Volume: 21
Issue Number: 26
First Page: 3095
Last Page: 3106
Page Count: 12
DOI: 10.2174/0929867321666140601195940
Price: $58
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