Curcumal Oil Attenuates Accelerated Atherosclerosis and Macrophage Foam Cell Formation by Modulating Genes Involved in Plaque Stability, Lipid Homeostasis and Inflammation

Abstract

In the present study, the anti-atherosclerotic effect and underlying mechanism of curcuma oil (C.oil), a lipophilic fraction from turmeric (Curcuma longa L.), was evaluated in a hamster model of accelerated atherosclerosis and in THP-1 macrophages. Male golden Syrian hamsters were subjected to partial carotid ligation (PCL) or ferric chloride induced arterial oxidative injury (Ox-injury) after 1 week of high-cholesterol (HC) diet or HC diet plus C. oil (100, 300mg/kg, per oral) treatment. The HC diet was continued and animals were analyzed after 1, 3 and 5 weeks of carotid injury. The C.oil fed group on HC diet was analyzed at 5 weeks. In hyperlipidaemic hamsters with PCL or Ox-injury, C.oil (300mg/kg) reduced elevated plasma and aortic lipids, arterial macrophage accumulation, and stenosis when compared to arterial injury alone. Similar group comparisons showed that elevated mRNA transcripts of MMP-2,-9, CD45, TNFα, IFNγ, IL-1β, and IL-6 in the atherosclerotic arteries were reduced while TGFβ and IL-10 were increased after C.oil treatment (300mg/kg). C.oil prevented HC diet- and OxLDL-induced lipid accumulation, decreased CD68 and CD36 mRNA expression, and augmented PPARα, LXRα, ABCA1 ABCG1 mRNA expression in both hyperlipidaemic hamster derived peritoneal and THP-1 macrophages. C.oil suppressed mRNA expression of TNFα, IL-1β, IL-6, and IFN-γ and increased TGFβ expression in peritoneal macrophages. In THP-1 macrophages, C.oil prevented OxLDL-induced TNF and IL-1β production and increased TGFβ levels. In the present study C.oil attenuated arterial injury-induced accelerated atherosclerosis, inflammation and macrophage foam cell formation.