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Review
. 2022 Oct 3:13:954938.
doi: 10.3389/fphar.2022.954938. eCollection 2022.

Roles and mechanisms of garlic and its extracts on atherosclerosis: A review

Affiliations
Review

Roles and mechanisms of garlic and its extracts on atherosclerosis: A review

Min Li et al. Front Pharmacol. .

Abstract

The prevention and treatment of cardiovascular diseases (CVDs) have achieved initial results, but the number of CVDs patients will increase rapidly in the next 10 years. Atherosclerosis (AS) is a significant risk factor for CVDs. The impact of lifestyle and daily diet varies considerably between different countries and continents and has been shown to affect the development of various diseases such as diabetes and CVDs. Primary and secondary prevention using alternative supplements and methods to avoid or reduce the use of traditional pharmacological drugs have also become popular. One of the reasons for this is that pharmacological drugs with lipid-lowering, and blood pressure-lowering effects cause many side effects that may negatively impact the quality of life. Patients are now emphasizing reliance on lifestyle changes to reduce cardiovascular risks. Garlic is a medicinal and edible plant that has been used for a long time. In order to reveal garlic application in the prevention and treatment of AS, reviewing the latest domestic and international studies through searching databases. The result shows that the antiatherogenic role of garlic is eximious. And the mechanisms are mainly related to hypolipidemic, antioxidant, antithrombotic, inhibiting angiogenesis, protecting endothelial cells, anti-inflammatory, anti-apoptotic, inhibiting vascular smooth muscle proliferation, and regulating gut microbiota. The main signaling pathways involve AMPK/TLRs, Keap1/Nrf2, PI3K/AKT, PPARγ/LXRα, GEF-H1/RhoA/Rac, etc. The antiatherogenic actions and molecular mechanism of garlic were reviewed in this study to obtain a robust evidence basis for the clinical application and mechanistic study and provide a theoretical basis for further utilization of garlic.

Keywords: Allium sativum; atherosclerosis; endothelial dysfunction; garlic; inflammation; oxidative stress.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Summary of the literature search process.
FIGURE 2
FIGURE 2
(A) Garlic plants. (B) Garlic bulbs. (C) Peeled garlic cloves.
FIGURE 3
FIGURE 3
The representative sulfur compounds of garlic.
FIGURE 4
FIGURE 4
Other compounds of garlic.
FIGURE 5
FIGURE 5
Mechanisms of the protective role of garlic in the treatment of atherosclerosis. ACAT, cholesterol acyltransferase; CEH, Cholesteryl ester hydrolase; LCAT, Lecithin cholesterol acyltransferase; LPL, Lipoprotein lipase; HL, Hepatic lipase; MTP, Microsomal triglyceride transfer protein; ABCA1, ATP Binding Cassette Subfamily A Member 1; HMGCR, Hydroxy-3-methyl glutaryl coenzyme A reductase; AMPK, AMP-activated protein kinase; FAS, Fatty acid synthase; SREBP, Sterol regulatory element-binding protein; TLR, Toll-like receptors; CRP, C-reaction protein; PPARγ, Peroxisome proliferator-activated receptor Gamma; LXRα, Liver X receptor α; IL-10, Interleukin-10; SHIP1, Src homology-2-containing inositol 5′-phosphatase 1; STAT3, Signal transducer and activator of transcription 3; Arg1, Arginase1; IRAK4, Interleukin-1 receptor-activated kinase 4; NF-κB, Nuclear factor kappa-B; IFN-g, Interferon gamma; NADPH, Nicotinamide adenine dinucleotide phosphate; PARP, Poly adenosine diphosphate-ribose polymerase; MMPs, Matrix metalloproteinases; TNF-α, Tumor necrosis factor-α; Fas, Fatty acid synthase; Bax, BCL2-Associated X; Bid, Recombinant Human BH3-Interacting Domain Death Agonist; Bcl-2, B-cell lymphoma-2; CaSR, Calcium-sensing receptor; eNOS, Endothelin nitric oxide synthase; ICAM-1, Intercellular cell adhesion molecule-1; VCAM-1, Vascular Cell Adhesion Molecule 1; ERK1/2, Extracellular regulated protein kinases; bFGF, Basic fibroblast growth factor; VEGF, Vascular endothelial growth factor; SIRT1, Sirtuin 1; ROS, Reactive oxygen species; PAI-1, Plasminogen Activator Inhibitor-1; GSH, Glutathione; SOD, Superoxide Dismutase; NQO1, NAD(P)H:quinone oxidoreductase 1; γ-GCSc, γ -glutamylcysteine synthetase antibody; SOD-1, Superoxide Dismutase 1; MDA, Malondialdehyde; TXB2, Thromboxane B2.

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