To investigate the role and mechanism of sulforaphane (SFN) in vascular calcification induced by oxidative stress.

The uremic vascular calcification model was established by treating rat vascular smooth muscle cells (RASMCs) with β-glycerophosphate. RASMCs were divided into 6 groups: normal control (NC) group, 1 μmol/L SFN group, 5 μmol/L SFN group, calcification group, 1 μmol/L SFN+calcification group, 5 μmol/L SFN+calcification group, and were all cultured for 72 h. Cell viability was measured by MTT. RASMCs calcification was visualized by Von Kossa staining. Calcium content was quantified by the microplate test, and mRNA level of FGF-23 was tested by real-time PCR. The expressions of OPN, Runx-2, Nrf-2 and Sirt-1 were evaluated by Western blotting. Confocal microscope was employed to observe mitochondria damage in RASMCs and the production of ROS in RASMCs was measured by reactive oxygen species assay.

(1) SFN did not affect cell viability of the NC group, but both low dosage and high dosage increased the cell viability of calcification group (all P<0.05). (2) Compared with calcification group, SNF treatment decreased the calcium concentration, intracellular calcium deposition and the mRNA level of FGF-23 (all P<0.05). (3) Compared with calcification group, SNF treatment decreased the fluorensence intensity, mitochondria injury and the protein expressions of OPN and Runx-2, but increased the protein expressions of Nrf-2, Sirt-1 and cleaved caspase-3 (all P<0.05).

SNF can effectively protect RASMCs against vascular calcification induced by oxidative stress, since it prevents the ROS production and mitochondria dysfunction through Nrf-2 and Sirt-1.

Oxidative stress; Vascular calcification; Nrf-2; Sirt-1; Sulforaphane