Andrographolide, a novel NF-κB inhibitor, inhibits vascular smooth muscle cell proliferation and cerebral endothelial cell inflammation

Chao Chien Chang, Yeh Fang Duann, Ting Lin Yen, Yu Ying Chen, Thanasekaran Jayakumar, Eng Thiam Ong, Joen Rong Sheu

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Background: Aberrant vascular smooth muscle cell (VSMC) proliferation and cerebral endothelial cell (CEC) dysfunction contribute significantly in the pathogenesis of cardiovascular diseases. Therefore, inhibition of these cellular events would be by candidate agents for treating these diseases. In the present study, the mechanism of anti-proliferative and anti-inflammatory effects of andrographolides, a novel nuclear factor-κB inhibitor, was investigated in VSMC and CEC cells. Methods: VSMCs and CECs were isolated from rat artery and mouse brain, respectively, and cultured before experimentation. The effect of andro on platelet-derived growth factor-BB (PDGF-BB) induced VSMC cell proliferation was evaluated by cell number, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression of extracellular signal regulated kinase 1/2 (ERK1/2), proliferating cell nuclear antigen (PCNA), and the effects on lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS) and, cyclooxygenase-2 (COX2) were detected byWestern blotting. Results: Andro significantly inhibited PDGF-BB (10 ng/ml) induced cell proliferation in a concentration (20-100 μM) dependent manner, which may be due to reducing the expression of ERK1/2, and by inhibiting the expression of PCNA. Andro also remarkably diminished LPS-induced iNOS and COX2 expression. Conclusions: The results of this study suggested that the effects of andro against VSMCs proliferation and CECs dysfunction may represent a promising approach for treatment of vascular diseases.

Original languageEnglish
Pages (from-to)308-315
Number of pages8
JournalActa Cardiologica Sinica
Volume30
Issue number4
Publication statusPublished - Jul 1 2014

Fingerprint

Vascular Smooth Muscle
Smooth Muscle Myocytes
Mitogen-Activated Protein Kinase 3
Endothelial Cells
Mitogen-Activated Protein Kinase 1
Cell Proliferation
Proliferating Cell Nuclear Antigen
Nitric Oxide Synthase Type II
Cyclooxygenase 2
Inflammation
Lipopolysaccharides
Vascular Diseases
Anti-Inflammatory Agents
Cardiovascular Diseases
Arteries
Cell Count
Brain
andrographolide
platelet-derived growth factor BB

Keywords

  • Andrographolide
  • CECs
  • COX2/iNOS
  • ERK/PCNA
  • LPS
  • PDGF-BB
  • VSMCs

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Andrographolide, a novel NF-κB inhibitor, inhibits vascular smooth muscle cell proliferation and cerebral endothelial cell inflammation. / Chang, Chao Chien; Duann, Yeh Fang; Yen, Ting Lin; Chen, Yu Ying; Jayakumar, Thanasekaran; Ong, Eng Thiam; Sheu, Joen Rong.

In: Acta Cardiologica Sinica, Vol. 30, No. 4, 01.07.2014, p. 308-315.

Research output: Contribution to journalArticle

Chang, Chao Chien ; Duann, Yeh Fang ; Yen, Ting Lin ; Chen, Yu Ying ; Jayakumar, Thanasekaran ; Ong, Eng Thiam ; Sheu, Joen Rong. / Andrographolide, a novel NF-κB inhibitor, inhibits vascular smooth muscle cell proliferation and cerebral endothelial cell inflammation. In: Acta Cardiologica Sinica. 2014 ; Vol. 30, No. 4. pp. 308-315.
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AU - Chang, Chao Chien

AU - Duann, Yeh Fang

AU - Yen, Ting Lin

AU - Chen, Yu Ying

AU - Jayakumar, Thanasekaran

AU - Ong, Eng Thiam

AU - Sheu, Joen Rong

PY - 2014/7/1

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N2 - Background: Aberrant vascular smooth muscle cell (VSMC) proliferation and cerebral endothelial cell (CEC) dysfunction contribute significantly in the pathogenesis of cardiovascular diseases. Therefore, inhibition of these cellular events would be by candidate agents for treating these diseases. In the present study, the mechanism of anti-proliferative and anti-inflammatory effects of andrographolides, a novel nuclear factor-κB inhibitor, was investigated in VSMC and CEC cells. Methods: VSMCs and CECs were isolated from rat artery and mouse brain, respectively, and cultured before experimentation. The effect of andro on platelet-derived growth factor-BB (PDGF-BB) induced VSMC cell proliferation was evaluated by cell number, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression of extracellular signal regulated kinase 1/2 (ERK1/2), proliferating cell nuclear antigen (PCNA), and the effects on lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS) and, cyclooxygenase-2 (COX2) were detected byWestern blotting. Results: Andro significantly inhibited PDGF-BB (10 ng/ml) induced cell proliferation in a concentration (20-100 μM) dependent manner, which may be due to reducing the expression of ERK1/2, and by inhibiting the expression of PCNA. Andro also remarkably diminished LPS-induced iNOS and COX2 expression. Conclusions: The results of this study suggested that the effects of andro against VSMCs proliferation and CECs dysfunction may represent a promising approach for treatment of vascular diseases.

AB - Background: Aberrant vascular smooth muscle cell (VSMC) proliferation and cerebral endothelial cell (CEC) dysfunction contribute significantly in the pathogenesis of cardiovascular diseases. Therefore, inhibition of these cellular events would be by candidate agents for treating these diseases. In the present study, the mechanism of anti-proliferative and anti-inflammatory effects of andrographolides, a novel nuclear factor-κB inhibitor, was investigated in VSMC and CEC cells. Methods: VSMCs and CECs were isolated from rat artery and mouse brain, respectively, and cultured before experimentation. The effect of andro on platelet-derived growth factor-BB (PDGF-BB) induced VSMC cell proliferation was evaluated by cell number, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression of extracellular signal regulated kinase 1/2 (ERK1/2), proliferating cell nuclear antigen (PCNA), and the effects on lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS) and, cyclooxygenase-2 (COX2) were detected byWestern blotting. Results: Andro significantly inhibited PDGF-BB (10 ng/ml) induced cell proliferation in a concentration (20-100 μM) dependent manner, which may be due to reducing the expression of ERK1/2, and by inhibiting the expression of PCNA. Andro also remarkably diminished LPS-induced iNOS and COX2 expression. Conclusions: The results of this study suggested that the effects of andro against VSMCs proliferation and CECs dysfunction may represent a promising approach for treatment of vascular diseases.

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KW - ERK/PCNA

KW - LPS

KW - PDGF-BB

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