Review Article

Therapeutic Potential of Quercetin as an Antiatherosclerotic Agent in Atherosclerotic Cardiovascular Disease: A Review

Table 1

Summary of the main effects of quercetin on antiatherosclerosis in vivo.

EffectSubjectsPossible mechanismReference

Animals
Endothelial protectionWistar ratsNeutralize ROS, protect mitochondrial membrane, reduce LPO, and increase GSH levels through the increased catalase activity[109]
ApoE−/− miceRegulate NADPH oxidase subunits expression[16]
Sprague-Dawley ratsIncrease GSH, erythrocyte CAT, and MDA levels[50]
Wistar ratsDecrease serum LDL, TC, MDA, and ROS to improve the vascular structure and prevent from the plaque formation[101]

Anti-inflammationApoE−/− miceDecrease serum TNF-α and IL-6 levels and increase levels[110]
ApoE−/− miceInhibit phenotypic and functional maturation of DCs[111]
Balb/c miceMediate HDL function and lipid-glucose state in the circulation by improving biological activity (quality) and the activity of bound to PON1[112]

AntiapoptosisNude miceActivate ERK and the ERK signaling pathway to promote autophagy[113]
ApoE−/− miceEnhance autophagy and downregulate mTOR, P53 and P21 protein expression levels to alleviate AS lesions and reduce lipid accumulation and increase ratio of LC3 II/I[83]

Regulate lipid metabolism and reduce the atherosclerotic plaque areaApoE−/− miceIncrease ABCA1 and LXRα expression and downregulate PCSK9 protein expression[110]
Wistar ratsElevate activity of hepatic CYP7A1, LXRα, and ABCG1 to promote cholesterol-to-bile acid conversion and cholesterol efflux[114]
C57BL/6J miceUpregulate LDLR and CYP7A1 gene expression to facilitate the removal of cholesterol via fecal excretion[115]
Wistar ratsPromote conversion of cholesterol to bile acids and cholesterol efflux by increasing hepatic CYP7A1 activity and hepatic LXRα, ABCG1, and LDLR protein expressions[116]
ApoE−/− miceElevate cholesterol accepting ability of HDL and increase ABCA1/G1 expression levels of proteins related to RCT[117]
Sprague-Dawley ratsInfluence gene and protein expression of SREBP1c and HMGR to lower lipid[118]
Sprague-Dawley ratsUpregulate hepatic gene expression CYP7A1, LXRα, ABCA1, and ABCG1 to promote cholesterol efflux[119]
Zucker ratsLower the level of HDL cholesterol and increase phosphorus level by increasing the ratio of ASAT/ALAT activity induced by leptin[56]
ApoE−/− miceRegulate expressions of ABCA1, LXRα, and PCSK9[26]
ApoE−/− miceDownregulate PCSK9 and CD36 protein expression and upregulate PPAR γ, LXRα, and ABCA1 protein expression levels in both the aortic and liver tissues[65]

Alter the gut microbiotaApoE−/− miceRegulate primary bile acid biosynthesis[95]
C57BL/6J miceImprove composition and functionality of gut microbiome and production of short chain fatty acids[120]
Wistar ratsStimulate bacterial enzymatic activity and increase enzymatic activity of the intestinal microbiota[121]
Ldlr−/− miceReduce MDA, cholesterol, and LPC 18 : 1 and increase IL-6 and coprostanol levels[98]

Humans
Anti-inflammationHealthy nonsmokersInhibit production of IL-1β, TNF-α, IL-6, and IL-8 in Lipopolysaccharide-stimulated[122]
CVD patientsDecrease transcriptional activity of NF-kB[74]
Endothelial protectionCVD individualsEnhance NO bioavailability, possibly by stimulating eNOS activity[123]