Potential mechanisms underlying the protective effects of salvianic acid A against atherosclerosis in vivo and vitro

This study examines the protective mechanisms of SAA on AS in vivo and in vitro. SAA treatment (3 and 10 mg/kg/d) prevented the progression of atherosclerotic lesions and decreased 58.2% and 72.8% of the lipid deposition in the aorta of high fat-diet-induced AS rat. Notably, SAA treatment ameliorated serum lipid abnormalities by decreasing 20.4% and 33.8% of triglyceride, 26.1% and 32.7% of total cholesterol, 36.0% and 57.3% of low-density lipoprotein-cholesterol levels and increasing 183.4% and 337.5% of high-density lipoprotein-cholesterol level in the serum of AS rat (all P <  0.05). SAA treatment lowered pro-inflammatory mediators including interleukin-1β, interleukin-6, tumor necrosis factor-α, intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) (all P <  0.05) by inhibiting the toll-like receptor 4/nuclear factor kappa B pathway. In addition, SAA treatment significantly decreased oxidative stress by increasing antioxidant enzymes activity, upregulating nuclear factor erythroid 2-related factor 2/heme oxygenase-1 pathway and downregulated expression of p47phox and p22phox (all P <  0.05) in vivo. Furthermore, SAA (10−5 and 3 × 10−5 M) suppressed oxidized low-density lipoprotein-induced expression of lectin-like oxidized low-density lipoprotein receptor-1, the phosphorylation of nuclear factor kappa B (p65), ICAM-1 and VCAM-1 (all P <  0.05) and inhibited NADPH oxidase subunit 4-mediat...
Source: Biomedicine and Pharmacotherapy - Category: Drugs & Pharmacology Source Type: research