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Angiotensin II (Ang II) is involved in the pathogenic progress of cardiovascular diseases via the promotion of abnormal proliferation and migration of human vascular smooth muscle cells (HVSMCs). Sulforaphane (SFN) exerts potent anti-inflammatory effects both in vitro and in vivo . In the present study, we aimed to investigate the effects of SFN on Ang II-induced abnormal migration of HVSMCs as well as the underlying mechanisms of those effects. The results showed that Ang II-induced HVSMC proliferation and migration were inhibited by treatment with SFN. SFN also exhibited anti-inflammatory activity, as indicated by its reduction of monocyte adhesion to HVSMCs via the reduction of ICAM1 and VCAM1 levels. Moreover, SFN reduced the Ang II-induced upregulation of HVSMC migration; this effect was inhibited by pretreatment with inhibitors of NADPH oxidase and ROS or transfection with siNOX4. In addition, SFN reversed the Ang II-induced upregulation of HVSMC migration via elevation of Nrf2 activation and expression. Taken together, the results indicate that SFN reverses Ang II-induced HVSMC migration through suppression of the NOX4/ROS/Nrf2 pathway. Thus, SFN is a potential agent to reverse the pathological changes involved in various cardiovascular diseases.

Sulforaphane Attenuates Angiotensin II-Induced Vascular Smooth Muscle Cell Migration via Suppression of NOX4/ROS/Nrf2 Signaling