This is further confirmed by the very

This is further confirmed by the very significant decrease in MDA level by Trévo™ and its positive effect on catalase and SOD. In the present study, the decreased level of GSH has been associated with elevations in the levels of end products (MDA) of lipid peroxidation in acetaminophen control. The increase in MDA level in liver suggests enhanced lipid peroxidation leading to tissue damage and failure of antioxidant defense mechanisms to prevent formation of excessive free radicals. SOD has been reported as one of the most important enzymes in the enzymatic antioxidant defense system [40]. Catalase is widely distributed in all animal tissue and the highest activity is found in the red purchase RPC1063 and in liver [41]. SOD offers protection from highly reactive superoxide radical and converts them to form H2O2 and O2 with H2O2 being further decomposed to H2O by catalase and GPx [42]. Supplements could enhance and augment the coordinate actions of various cellular antioxidants in mammalian cells, which are critical for effectively detoxifying free radicals, by contributing components that possess intrinsic antioxidant activity or those that potentiate the activity of other antioxidative factors in the antioxidant network.
Conflict of interest
Introduction Hypercholesterolemia and oxidative stress represent the major risk factors for the development and progression of atherosclerosis and related cardiovascular diseases [1,2]. A number of experimental studies have clearly demonstrated that high plasma LDL-cholesterol levels are positively correlated with atherosclerosis process [3]. However, HDL-cholesterol is an antiatherogenic fraction [4]. In addition, a long-standing relationship exists between high plasma triglyceride levels and cardiovascular disease [5]. Lifestyle and dietary habits are crucial in the prevention of some human diseases such as hyperlipidemia and atherosclerosis. Indeed, the Mediterranean diet rich in fruits and vegetables is negatively correlated with cardiovascular risk [6]. Thus, the management of hyperlipidemia needs a strategy based on diet control and hypolipidemic treatment [7]. In this context, it is very important to search functional foods and dietary phytochemicals with hypolipidemic and antioxidant virtues, because hyperlipidemia and low density lipoprotein oxidation are known to be the key process in the physiopathology of atherosclerosis which can be treated by hypolipidemic and antioxidant therapies [3]. Sweet basil (Ocimum basilicum) from Lamiaceae family is an aromatic plant cultivated as a culinary herb, condiment or spice and as food aromatizing [11]. In the east of Morocco, sweet basil is not only used for cooking but also considered as medicinal plant to treat hyperlipidaemia, atherosclerosis and related pathologies. Recently, sweet basil has been proved to demonstrate a number of biological activities, such as antidiabetic [12] and anti thrombotic effects [13]. In the present study we demonstrated that the phenolic acid-rich extract from O. basilicum exerted a significant hypolipidemic activity in Triton WR-1339-induced hyperlipemic mice and prevents efficiently against lipoprotein-rich plasma oxidation. This results could be used to develop natural antiatherogenic treatments from sweet basil.
Materials and methods
Results
Discussion The development of hyperlipidemia in animal models by using Triton WR-1339 is a strategy widely followed in a number of experimental studies [17]. This nonionic surfactant inhibits the enzymatic activity of lipoprotein lipase, resulting in the accumulation of total cholesterol, triglycerides and very low density lipoprotein in plasma [18]. In the present work, we followed the same strategy using a murine model injected with Triton WR-1339 to investigate the hypolipidemic effect of phenolic extract from O. basilicum. We observed that the extract significantly decreased the mice plasma total cholesterol. This activity was associated with a diminution in LDL-cholesterol representing the atherogenic fraction [19]. As demonstrated by Mbikay et al., [20], this finding led us to suggest that the cholesterol-lowering activity of the phenolic extract might be due to the activation of LDL hepatic receptors (B/E) for the final clearance as bile acids. We suggest also, on the basis of other studies, that the hypolipidemic effect can be explained by other mechanisms involving modulation of enzymes implicated in cholesterol metabolism: HMG-CoA reductase [21], acyl CoA cholesterol acyl transferase (ACAT) [22] and lecithin-cholesterol acyl transferase (LCAT) [23].