Dietary canolol protects the heart against the deleterious effects induced by the association of rapeseed oil, vitamin E and coenzyme Q10 in the context of a high-fat diet

Abstract

BackgroundObesity progressively leads to cardiac failure. Omega-3 polyunsaturated fatty acids (PUFA) have been shown to have cardio-protective effects in numerous pathological situations. It is not known whether rapeseed oil, which contains α-linolenic acid (ALA), has a similar protective effect. Omega-3 PUFAs are sensitive to attack by reactive oxygen species (ROS), and lipid peroxidation products could damage cardiac cells. We thus tested whether dietary refined rapeseed oil (RSO) associated with or without different antioxidants (vitamin E, coenzyme Q10 and canolol) is cardio-protective in a situation of abdominal obesity.MethodsSixty male Wistar rats were subdivided into 5 groups. Each group was fed a specific diet for 11 weeks: a low-fat diet (3% of lipids, C diet) with compositionally-balanced PUFAs; a high-fat diet rich in palm oil (30% of lipids, PS diet); the PS diet in which 40% of lipids were replaced by RSO (R diet); the R diet supplemented with coenzyme Q10 (CoQ10) and vitamin E (RTC diet); and the RTC diet supplemented with canolol (RTCC diet). At the end of the diet period, the rats were sacrificed and the heart was collected and immediately frozen. Fatty acid composition of cardiac phospholipids was then determined. Several features of cardiac function (fibrosis, inflammation, oxidative stress, apoptosis, metabolism, mitochondrial biogenesis) were also estimated.ResultsAbdominal obesity reduced cardiac oxidative stress and apoptosis rate by increasing the proportion of arachidonic acid (AA) in membrane phospholipids. Dietary RSO had the same effect, though it normalized the proportion of AA. Adding vitamin E and CoQ10 in the RSO-rich high fat diet had a deleterious effect, increasing fibrosis by increasing angiotensin-2 receptor-1b (Ag2R-1b) mRNA expression. Overexpression of these receptors triggers coronary vasoconstriction, which probably induced ischemia. Canolol supplementation counteracted this deleterious effect by reducing coronary vasoconstriction.ConclusionCanolol was found to counteract the fibrotic effects of vitamin E + CoQ10 on cardiac fibrosis in the context of a high-fat diet enriched with RSO. This effect occurred through a restoration of cardiac Ag2R-1b mRNA expression and decreased ischemia.

Effect of Rosmarinic Acid and Sinapic Acid on Oxidative Stress Parameters in the Cardiac Tissue and Serum of Type 2 Diabetic Female Rats

“…Similarly to palm oil-rich diet, the diet rich in lard also effected in an increase of AA in the heart membrane [91]. The authors suggest that AA has a strong effect on vessel dilatation and its accumulation may promote coronary flow, which can result in an increased mechanical function of the heart [90].…”

“…Only few publications indicate that TBARS level does not change or decreases in the cardiac tissue in diabetic rodents [61,89]. The lowered TBARS level in the heart was observed by the authors, who fed the rats with high-fat diet (with 30% of fat from palm oil) for 11 weeks [90]. These authors explain the result by changes in polyunsaturated fatty acids (PUFA) profile in phospholipids of the heart membrane-there was a significant increase in arachidonic acid (AA) in the heart membrane of rats on palm oil-rich diet, compared to the membrane of rats fed with standard chow [90].…”

The Effect of a High-Fat Diet on the Fatty Acid Composition in the Hearts of Mice

“…Similarly, the protein carbonyl content in heart tissue did not differ between SD and HFD mice. Moreover, Leger et al [85] found that HFD led to decrease of cardiac oxidative stress and apoptosis rate in rats. This was associated with increased arachidonic acid proportion in membrane phospholipids.…”

EPA Is Cardioprotective in Male Rats Subjected to Sepsis, but ALA is Not Beneficial

“…Dietary EPA is protective during sepsis, but we do not know whether other n-3 PUFAs such as α-linolenic (C18:3 n-3 or ALA) acid is efficient. Indeed, in contrast with dietary EPA, ALA does not allow the easy accumulation of EPA in membrane phospholipids [20]. Phospholipid EPA is directly accessible to the cyclooxygenase enzyme via the action of phospholipase A2.…”