Abstract Title:

Inhibitory role of magnolol on proliferative capacity and matrix metalloproteinase-9 expression in TNF-alpha-induced vascular smooth muscle cells.

Abstract Source:

Int Immunopharmacol. 2007 Aug ;7(8):1083-91. Epub 2007 May 4. PMID: 17570325

Abstract Author(s):

Hong-Man Kim, Sung-Jin Bae, Dong-Wook Kim, Bo-Kyung Kim, Soo-Bok Lee, Ung-Soo Lee, Cheorl-Ho Kim, Sung-Kwon Moon

Article Affiliation:

Hong-Man Kim


Magnolol, an active component extracted from Magnolia officinalis, has been reported to inhibit the development of atherosclerotic disease. However, it is not known whether magnolol exerts similar cardioprotective effects in cells treated with TNF-alpha. In the present study, magnolol treatment was found to show potent inhibitory effects on cell proliferation in cultured VSMC in the presence of TNF-alpha. These inhibitory effects were associated with reduced extracellular signal-regulated kinase (ERK) 1/2 activity and G1 cell cycle arrest. Magnolol treatment strongly induced the expression of p21WAF1, but resulted in a decrease in cyclin-dependent kinases (CDKs) and cyclins involved in G1 progression. In addition to G1 cell cycle arrest and growth inhibition in VSMC, magnolol also caused the strong inhibition of TNF-alpha-induced matrix metalloproteinase-9 (MMP-9) expression in a dose-dependent manner as determined by zymography and immunoblot. Moreover, magnolol treatment strongly decreased MMP-9 promoter activity in response to TNF-alpha. We further demonstrated that magnolol reduced the transcriptional activity of NF-kappaB and activation protein-1 (AP-1), two important nuclear transcription factors that are involved in MMP-9 expression. Collectively, these results show that magnolol inhibits cell proliferation, G1 to S phase cell cycle progress and MMP-9 expression through the transcription factors NF-kappaB and AP-1 in TNF-alpha-induced VSMC. The findings of the present study reveal a potential mechanism that explains the anti-atherogenic activity of magnolol.

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