Elucidating the inhibitory mechanisms of magnolol on rat smooth muscle cell proliferation

Chieh Hsi Wu, Chih Wen Chen, Ho Chih Chen, Weng Cheng Chang, Min Ji Shu, Jui Sung Hung

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)


The pathological mechanism of percutaneous transluminal coronary angioplasty-induced restenosis has been attributed to outgrowth of vascular smooth muscle cells. Pretreatment with antioxidants has been shown to reduce restenosis. Magnolol, an active compound of Magnolia officinalis, has exhibited approximately 1,000 times more potent antioxidant effects than alpha-tocopherol. In this study, we demonstrate, using cytometric analysis, an approximate 61% reduction of smooth muscle cells progressing to the S-phase by 0.05 mg/ml of magnolol. A BrdU incorporation assay also showed a significant reduction (73%) of DNA synthesis using 0.05 mg/ml of magnolol. The protein level of the proliferating cell nuclear antigen was suppressed by approximately 48% using 0.05 mg/ml of magnolol. This was in agreement with the promoter activity of nuclear factor-kappa B, which was also attenuated by 0.05 mg/ml of magnolol. Since receptor interacting protein and caspase-3 protein expression levels were both increased by magnolol in a dose-dependent manner, the apoptotic pathway may mediate the inhibition of cell growth. Our finding that malondialdehyde formation was significantly inhibited by 0.05 mg/ml of magnolol further supported the antioxidant effect of magnolol. These studies suggest that magnolol might be a potential pharmacological reagent in preventing balloon injury-induced restenosis.

Original languageEnglish
Pages (from-to)392-399
Number of pages8
JournalJournal of Pharmacological Sciences
Issue number4
Publication statusPublished - 2005
Externally publishedYes


  • Magnolol
  • Neointima formation
  • Percutaneous transluminal coronary angioplasty
  • Restenosis

ASJC Scopus subject areas

  • Pharmacology


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