Allicin induced vasorelaxation via endothelium‑dependent and endothelium‑independent mechanisms

Abstract

Allicin is the active content of garlic which produced the protective effects against cardiovascular diseases. Vascular contraction and relaxation are the essential capacities of vascular to maintain the normal function. Endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are the main cell types to control vascular functions. In order to observe the effects of allicin on vascular function and explore the potential regulation mechanisms. Mass spectrometry analysis was used to search the potential downstream targets of allicin in artery. A primary culture of mouse VSMCs and ECs was established by enzymatic digestion of aorta. Small interfering RNA was used to knock down the expression of target gene, and vector was used to upregulate specific protein expression. Protein levels were detected by Western blot. Our results showed that allicin treatment increased both endothelium-dependent and endothelium-independent relaxation in aortic rings. According to mass spectrometry analysis, we proposed that ATP-binding cassette transporter G1 (ABCG1), ryanodine receptor 2 (RyR2) and peroxisome proliferator-activated receptor γ (PPAR γ) might the downstream targets of allicin. Allicin increased ABCG1 expression and nitric oxide (NO) production in ECs, ABCG1 siRNA decreased allicin-induced NO production. RyR2 expression and Ca2+ spark were inhibited by allicin in VSMCs, RyR2 overexpression partly reversed allicin-induced Ca2+ spark decrease in VSMCs. PPAR γ siRNA significantly inhibited the effects of allicin in ECs and VSMCs. These results indicated that allicin treatment produced vasorelaxation effect via increasing ABCG1 expression and NO production in ECs and reducing RyR2 expression and Ca2+ spark in VSMCs. PPAR γ signaling pathway was confirmed to mediate these processes.