Salvianolic acid B attenuates VCAM-1 and ICAM-1 expression in TNF-α-treated human aortic endothelial cells

Yung Hsiang Chen, Shing Jong Lin, Hung Hai Ku, Ming Shi Shiao, Feng Yen Lin, Jaw Wen Chen, Yuh Lien Chen

Research output: Contribution to journalArticle

149 Citations (Scopus)

Abstract

Attachment to, and migration of leukocytes into the vessel wall is an early event in atherogenesis. Expression of cell adhesion molecules by the arterial endothelium may play a major role in atherosclerosis. It has been suggested that antioxidants inhibit the expression of adhesion molecules and may thus attenuate the processes leading to atherosclerosis. In the present study, the effects of a potent water-soluble antioxidant, salvianolic acid B (Sal B), and an aqueous ethanolic extract (SME), both derived from a Chinese herb, Salvia miltiorrhiza, on the expression of endothelial-leukocyte adhesion molecules by tumor necrosis factor-α (TNF-α)-treated human aortic endothelial cells (HAECs) were investigated. When pretreated with SME (50 and 100 μg/ml), the TNF-α-induced expression of vascular adhesion molecule-1 (VCAM-1) was notably attenuated (77.2±3.2% and 80.0±2.2%, respectively); and with Sal B (1, 2.5, 5, 10, and 20 μg/ml), 84.5±1.9%, 78.8±1.2%, 58.9±0.4%, 58.7±0.9%, and 57.4±0.3%, respectively. Dose-dependent lowering of expression of intercellular cell adhesion molecule-1 (ICAM-1) was also seen with SME or Sal B. In contrast, the expression of endothelial cell selectin (E-selectin) was not affected. SME (50 μg/ml) or Sal B (5 μg/ml) significantly reduced the binding of the human monocytic cell line, U937, to TNF-α-stimulated HAECs (45.7±2.5% and 55.8±1.2%, respectively). SME or Sal B significantly inhibited TNF-α-induced activation of nuclear factor kappa B (NF-κB) in HAECs (0.36- and 0.48-fold, respectively). These results demonstrate that SME and Sal B have anti-inflammatory properties and may explain their anti-atherosclerotic properties. This new mechanism of action of Sal B and SME, in addition to their previously reported inhibition of LDL, may help explain their efficacy in the treatment of atherosclerosis.

Original languageEnglish
Pages (from-to)512-521
Number of pages10
JournalJournal of Cellular Biochemistry
Volume82
Issue number3
DOIs
Publication statusPublished - 2001
Externally publishedYes

Fingerprint

Endothelial cells
Cell Adhesion Molecules
Intercellular Adhesion Molecule-1
Blood Vessels
Endothelial Cells
Tumor Necrosis Factor-alpha
Atherosclerosis
Salvia miltiorrhiza
Adhesion
Antioxidants
Selectins
Molecules
NF-kappa B
Endothelium
human TNF protein
salvianolic acid B
Leukocytes
Anti-Inflammatory Agents
Chemical activation
Cells

Keywords

  • Atherosclerosis
  • E-selectin
  • Endothelial cell
  • ICAM-1
  • Salvianolic acid B (Sal B)
  • VCAM-1

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

Cite this

Salvianolic acid B attenuates VCAM-1 and ICAM-1 expression in TNF-α-treated human aortic endothelial cells. / Chen, Yung Hsiang; Lin, Shing Jong; Ku, Hung Hai; Shiao, Ming Shi; Lin, Feng Yen; Chen, Jaw Wen; Chen, Yuh Lien.

In: Journal of Cellular Biochemistry, Vol. 82, No. 3, 2001, p. 512-521.

Research output: Contribution to journalArticle

Chen, Yung Hsiang ; Lin, Shing Jong ; Ku, Hung Hai ; Shiao, Ming Shi ; Lin, Feng Yen ; Chen, Jaw Wen ; Chen, Yuh Lien. / Salvianolic acid B attenuates VCAM-1 and ICAM-1 expression in TNF-α-treated human aortic endothelial cells. In: Journal of Cellular Biochemistry. 2001 ; Vol. 82, No. 3. pp. 512-521.
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AU - Lin, Feng Yen

AU - Chen, Jaw Wen

AU - Chen, Yuh Lien

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N2 - Attachment to, and migration of leukocytes into the vessel wall is an early event in atherogenesis. Expression of cell adhesion molecules by the arterial endothelium may play a major role in atherosclerosis. It has been suggested that antioxidants inhibit the expression of adhesion molecules and may thus attenuate the processes leading to atherosclerosis. In the present study, the effects of a potent water-soluble antioxidant, salvianolic acid B (Sal B), and an aqueous ethanolic extract (SME), both derived from a Chinese herb, Salvia miltiorrhiza, on the expression of endothelial-leukocyte adhesion molecules by tumor necrosis factor-α (TNF-α)-treated human aortic endothelial cells (HAECs) were investigated. When pretreated with SME (50 and 100 μg/ml), the TNF-α-induced expression of vascular adhesion molecule-1 (VCAM-1) was notably attenuated (77.2±3.2% and 80.0±2.2%, respectively); and with Sal B (1, 2.5, 5, 10, and 20 μg/ml), 84.5±1.9%, 78.8±1.2%, 58.9±0.4%, 58.7±0.9%, and 57.4±0.3%, respectively. Dose-dependent lowering of expression of intercellular cell adhesion molecule-1 (ICAM-1) was also seen with SME or Sal B. In contrast, the expression of endothelial cell selectin (E-selectin) was not affected. SME (50 μg/ml) or Sal B (5 μg/ml) significantly reduced the binding of the human monocytic cell line, U937, to TNF-α-stimulated HAECs (45.7±2.5% and 55.8±1.2%, respectively). SME or Sal B significantly inhibited TNF-α-induced activation of nuclear factor kappa B (NF-κB) in HAECs (0.36- and 0.48-fold, respectively). These results demonstrate that SME and Sal B have anti-inflammatory properties and may explain their anti-atherosclerotic properties. This new mechanism of action of Sal B and SME, in addition to their previously reported inhibition of LDL, may help explain their efficacy in the treatment of atherosclerosis.

AB - Attachment to, and migration of leukocytes into the vessel wall is an early event in atherogenesis. Expression of cell adhesion molecules by the arterial endothelium may play a major role in atherosclerosis. It has been suggested that antioxidants inhibit the expression of adhesion molecules and may thus attenuate the processes leading to atherosclerosis. In the present study, the effects of a potent water-soluble antioxidant, salvianolic acid B (Sal B), and an aqueous ethanolic extract (SME), both derived from a Chinese herb, Salvia miltiorrhiza, on the expression of endothelial-leukocyte adhesion molecules by tumor necrosis factor-α (TNF-α)-treated human aortic endothelial cells (HAECs) were investigated. When pretreated with SME (50 and 100 μg/ml), the TNF-α-induced expression of vascular adhesion molecule-1 (VCAM-1) was notably attenuated (77.2±3.2% and 80.0±2.2%, respectively); and with Sal B (1, 2.5, 5, 10, and 20 μg/ml), 84.5±1.9%, 78.8±1.2%, 58.9±0.4%, 58.7±0.9%, and 57.4±0.3%, respectively. Dose-dependent lowering of expression of intercellular cell adhesion molecule-1 (ICAM-1) was also seen with SME or Sal B. In contrast, the expression of endothelial cell selectin (E-selectin) was not affected. SME (50 μg/ml) or Sal B (5 μg/ml) significantly reduced the binding of the human monocytic cell line, U937, to TNF-α-stimulated HAECs (45.7±2.5% and 55.8±1.2%, respectively). SME or Sal B significantly inhibited TNF-α-induced activation of nuclear factor kappa B (NF-κB) in HAECs (0.36- and 0.48-fold, respectively). These results demonstrate that SME and Sal B have anti-inflammatory properties and may explain their anti-atherosclerotic properties. This new mechanism of action of Sal B and SME, in addition to their previously reported inhibition of LDL, may help explain their efficacy in the treatment of atherosclerosis.

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