Abstract
Eugenol, a component of essential oils of medicinal and food plants, has a hypolipidemic effect in experimental animals although its mechanism of action is still unclear. This study aims to explore the mechanism of the hypolipidemic effect of eugenol in rats fed a high cholesterol and fat diet (HCFD). Eugenol significantly reduced total cholesterol (TC), low-density lipoproteins (LDL), atherogenic index (AI) but not high-density lipoproteins (HDL) or triglycerides (TG). Eugenol also decreased steatosis and hepatic inflammation in liver sections, decreased hepatomegaly, and the hepatic marker enzymes alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activity and increased the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) activity in hypercholesterolemic rats. Eugenol did not inhibit hepatic 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase but caused down-regulation of transient receptor potential vanilloid (TRPV1) channels in the liver. Docking simulation using fast, rigid exhaustive docking (FRED) software indicated a tail-up/head-down interaction of eugenol with TRPV1 channel. Data indicate that eugenol does not inhibit HMG-CoA reductase but rather induces its action by interaction with TRPV1 channels.
Highlights
Numerous biological activities of eugenol have been documented including antioxidant[1,6,7], anti-inflammatory[1,6,8], anti-aging[7], and anticancer activities[1]
Others suggested a direct interaction with the transient receptor potential vanilloid 1 (TRPV1) channel[18,19]
TRPV1 activation was found to be essential for capsaicin-induced energy expenditure, decreasing blood cholesterol level and treating hyperlipidemia[21,22]
Summary
Numerous biological activities of eugenol have been documented including antioxidant[1,6,7], anti-inflammatory[1,6,8], anti-aging[7], and anticancer activities[1]. Aspirin eugenol ester was synthesized and tested on hyperlipidemic rats. We hypothesized that the hypocholesterolemic effect of eugenol may be associated with the modulation of TRPV1 receptor. The rationale underlying this hypothesis is that eugenol, similar to capsaicin, contains a vanilloyl moiety and may act as an agonist activating TRPV1 receptor (Supplementary Fig. 1). The structural similarity of capsaicin and eugenol suggests that these two ligands may share the same molecular mechanism to produce their effects[18]. This study aims to investigate the role of TRPV1 receptor in the hypocholesterolemic and anti-steatotic effects of eugenol in a rat model. We provide the eugenol-TRPV1 possible interactions at the molecular level using computer modeling and docking technique
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