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 lipid profile as well as hypercholesterolemia indices. The induced hypercholesterolemia promoted the progression of atherosclerotic plaque with the occurrence of foam cells in bulging structures. Simultaneously, the treatments of curcumin and atorvastatin caused significant reductions in total cholesterol, LDL cholesterol, VLDL-cholesterol as well as hypercholesterolemia indices of the Castelli Risk Index-I & II and atherogenic indices. Accordingly, the treatments of curcumin and atorvastatin caused significant regression in atherogenic plaque area, total wall area, and increased lumen volume. Subsequently, the molecular docking showed significant interactions of curcumin and atorvastatin with HMG-CoA reductase which was depicted by bonding energy, numbers of H-bonds, and bond length. Accordingly, the ADMET and toxicity data revealed significant druggability of curcumin along with supportive analysis of BOILED 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.
Key words: Curcumin, HMG-CoA reductase, Molecular docking, ADMET, Atherosclerotic plaque, Castelli Indexes.
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