Emodin inhibits tumor necrosis factor-α-induced migration and inflammatory responses in rat aortic smooth muscle cells
- Authors:
- Published online on: March 15, 2012 https://doi.org/10.3892/ijmm.2012.940
- Pages: 999-1006
Metrics: Total
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
Abstract
Emodin, a naturally occurring anthraquinone derivative in oriental herbal medicine, has been shown to exert a variety of pharmacological activities. The goal of this study was to determine the effects of emodin on the modulation of cell proliferation, migration, inflammatory responses, and matrix metalloproteinase (MMP)-2 and MMP-9 expression in tumor necrosis factor (TNF)-α-induced rat aortic smooth muscle cells (RASMCs). Cell proliferation and migration were measured using the MTT assay and the transwell chamber assay, respectively. Quantitative real-time PCR and western blot analysis were used to detect MMP expression. Gel shift was used for analysis of nuclear factor (NF)-κB activation. In addition, the expression of several inflammatory genes was also analyzed. Treatment of RASMCs with emodin significantly and dose-dependently attenuated TNF-α-induced proliferation, migration, mRNA and protein expression of MMP-2 and MMP-9, and NF-κB activation. Furthermore, emodin significantly inhibited TNF-α-evoked inflammatory responses, as demonstrated by the reduction in the expression of inflammatory genes. These results suggest that emodin inhibits TNF-α-induced proliferation, migration, MMP-2 and MMP-9 expression as well as inflammatory responses in cultured RASMCs, supporting the notion that emodin may have potential application in clinical atherosclerosis disease.
