Atherosclerotic plaque regression and HMG-CoA reductase inhibition potential of curcumin: An integrative omics and in-vivo study

The current study was carried out to evaluate the potential of curcumin against the progression of atherosclerosis and cholesterol biosynthesis by incorporating the combined data of in-vivo assessments and integrative omics examinations. The high fat diet and supplementation of cholesterol powder caused significant alterations in the lipid profile as well as hypercholesterolemia indices. The induced hypercholesterolemia promoted progression of atherosclerotic plaque with the occurrence of foam cells in a bulged structure. Simultaneously, the treatments of curcumin and atorvastatin caused significant reductions in total cholesterol, low density lipoprotein cholesterol, and very low-density lipoprotein cholesterol, as well as hypercholesterolemia indices of Castelli Risk Index-I and II and atherogenic indices. Accordingly, the treatments of curcumin and atorvastatin caused significant regressions in atherogenic plaque area, total wall area, and increased lumen volume. Subsequently, molecular docking showed significant interactions of curcumin and atorvastatin with β-Hydroxy β-methylglutaryl-CoA reductase, which were depicted by bonding energy, number of H–bonds, and bond length. Accordingly, the absorption, distribution, metabolism, excretion, and toxicity and toxicity data revealed significant druggability of curcumin along with supportive analysis of Brain Or IntestinaL EstimateD-Egg prediction of gastrointestinal absorption. Thus, it can be illustrated that curcumin has significant potential to promote regression in atherosclerotic plaque and subside the cholesterol biosynthesis by inhibition of HMG-CoA reductase, as indicated by the outcomes.