Hyperhomocysteinemia is an independent risk factor for various vascular diseases. Several clues suggested that salidroside has therapeutic potential on homocysteine-related cardiovascular diseases. However, the underlying molecular mechanism is still under investigation.

Two observations are of enormously importance in our study. First, SAL alleviated the expression of p16 INK4A and p21CIP1 both in aorta and in HUVECs, possibly through decreasing the expression of inflammatory cytokines and upregulating the expression of SIRT3. Second, SAL attenuated the VSMCs proliferation and collagen deposition. These information are valuable for us to understand the protective effect of SAL on vascular, though the detailed underlying molecular mechanisms still need further investigation.