Sulforaphane inhibits smooth muscle cell proliferation and migration by reducing MMP-9 activity via the Ras and RhoA/ROCK pathways

• 10μM SFN was no cytotoxicity in A7r5 cells.
• SFN reduced the wound healing capability and migration of A7r5 cells.
• SFN were able to inhibit the MMP-9 expression of A7r5 cells.
• SFN attenuated the over-expression of actin cytoskeleton stimulated by TNF-α.
• SFN mediated A7r5 cells migration by suppressing the Ras and RhoA/ROCK signaling pathways.

Vascular smooth muscle cell (VSMC) proliferation and migration triggered by inflammatory stimuli are involved in the development and progression of atherosclerosis. Here, we investigate the capacity of sulforaphane (SFN) on TNF-α-induced proliferation, migration and signal transduction in A7r5 smooth muscle cells. SFN inhibited the migration ability of A7r5 cells induced by TNF-α using wound healing assay and Boyden chamber assay. After treatment of SFN at various concentrations with TNF-α, A7r5 cell reduced matrix metalloproteinase-9 (MMP-9) expression. Fluorescent phalloidin staining demonstrated that increased intense F-actin staining in the TNF-α-induced A7r5 cells was inhibited by SFN. The levels of Ras and RhoA/ROCK-related proteins in the TNF-α treated A7r5 cells were increased, whereas these protein expression were attenuated by SFN. The results suggested that SFN could mediate A7r5 cells migration by reducing MMP-9 activity involving the suppression of the Ras and RhoA signaling pathways.