title: Magnolol reduced TNF-α-induced vascular cell adhesion molecule-1 expression in endothelial cells via JNK/p38 and NF-κB signaling pathways.
abstract: Expression of cell adhesion molecules by the endothelium and the attachment of leukocytes to these cells play major roles in inflammation and cardiovascular disorders. Magnolol, a major active component of Magnolia officinalis, has antioxidative and anti-inflammatory properties. In the present study, the effects of magnolol on the expression of vascular cell adhesion molecule-1 (VCAM-1) in human aortic endothelial cells (HAECs) and the related mechanisms were investigated. TNF-α induced VCAM-1 protein expression and mRNA stability were significantly decreased in HAECs pre-treated with magnolol. Magnolol significantly reduced the phosphorylation of ERK, JNK, and p38 in TNF-α-treated HAECs. The decrease in VCAM-1 expression in response to TNF-α treatment was affected by JNK and p38 inhibitors, not by an ERK inhibitor. Magnolol also attenuates NF-κB activation and the translocation of HuR (an RNA binding protein) in TNF-α-stimulated HAECs. The VCAM-1 expression was weaker in the aortas of TNF-α-treated apo-E deficient mice with magnolol treatment. These data demonstrate that magnolol inhibits TNF-α-induced JNK/p38 phosphorylation, HuR translocation, NF-κB activation, and thereby suppresses VCAM-1 expression resulting in reduced leukocyte adhesion. Taken together, these results suggest that magnolol has an anti-inflammatory property and may play an important role in the prevention of atherosclerosis and inflammatory responses.
authors.affiliation: Department of Anatomy and Cell Biology, National Taiwan University, Taipei, Taiwan , Research Center for Industry of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan.
authors.forename: Chan-Jung
authors.initials: CJ
authors.lastname: Liang
authors.forename: Chiang-Wen
authors.initials: CW
authors.lastname: Lee
authors.forename: Hsin-Ching
authors.initials: HC
authors.lastname: Sung
authors.forename: Yung-Hsiang
authors.initials: YH
authors.lastname: Chen
authors.forename: Shu-Huei
authors.initials: SH
authors.lastname: Wang
authors.forename: Pei-Jhen
authors.initials: PJ
authors.lastname: Wu
authors.forename: Yao-Chang
authors.initials: YC
authors.lastname: Chiang
authors.forename: Jaw-Shiun
authors.initials: JS
authors.lastname: Tsai
authors.forename: Chau-Chung
authors.initials: CC
authors.lastname: Wu
authors.forename: Chi-Yuan
authors.initials: CY
authors.lastname: Li
authors.forename: Yuh-Lien
authors.initials: YL
authors.lastname: Chen
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D001011:Aorta / Q000166:cytology / Q000187:drug effects; D001057:Apolipoproteins E / Q000172:deficiency; D050197:Atherosclerosis / Q000517:prevention & control; D001713:Biphenyl Compounds / Q000494:pharmacology*; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000378:metabolism*; D015870:Gene Expression / Q000187:drug effects* / Q000235:genetics*; D006801:Humans; D017705:Lignans / Q000494:pharmacology*; D020935:MAP Kinase Signaling System / Q000187:drug effects / Q000235:genetics* / Q000502:physiology*; D051379:Mice; D016328:NF-kappa B / Q000235:genetics* / Q000502:physiology*; D010766:Phosphorylation / Q000187:drug effects / Q000235:genetics; D008517:Phytotherapy; D015398:Signal Transduction / Q000187:drug effects / Q000235:genetics* / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000009:adverse effects*; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics* / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D001057:Apolipoproteins E; D001713:Biphenyl Compounds; D017705:Lignans; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; C005498:magnolol