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, 58 (6), 3472-8

Anti-inflammatory Bioactivities of Honokiol Through Inhibition of Protein Kinase C, Mitogen-Activated Protein Kinase, and the NF-kappaB Pathway to Reduce LPS-induced TNFalpha and NO Expression

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Anti-inflammatory Bioactivities of Honokiol Through Inhibition of Protein Kinase C, Mitogen-Activated Protein Kinase, and the NF-kappaB Pathway to Reduce LPS-induced TNFalpha and NO Expression

Louis Kuoping Chao et al. J Agric Food Chem.

Abstract

Much recent research has demonstrated that honokiol, a phenolic compound originally isolated from Magnolia officinalis, has potent anticancer activities; however, the detailed molecular mechanism of its anti-inflammatory activity has not yet been fully addressed. In this study we demonstrated that honokiol inhibited lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha secretion in macrophages, without affecting the activity of the tumor necrosis factor-alpha converting enzyme. At the same time, honokiol not only inhibited nitric oxide expression in LPS-stimulated murine macrophages but also inhibited the LPS-induced phosphorylation of ERK1/2, JNK1/2, and p38. By means of confocal microscope analysis we demonstrated that phosphorylation and membrane translocation of protein kinase C-alpha, as well as NF-kappaB activation, were inhibited by honokiol in LPS-stimulated macrophages. Furthermore, it was found that honokiol neither antagonizes the binding of LPS to cells nor alters the cell surface expression of toll-like receptor 4 and CD14. Our current results have exhaustively described the anti-inflammatory properties of honokiol, which could lead to the possibility of its future pharmaceutical application in the realm of immunomodulation.

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