Abstract
Scientific literature shows that inflammation and oxidative stress contribute in the pathogenesis of atherosclerosis. The oxidative stress is the consequence of an imbalance between the free radical generation and elimination. One source of free oxygen radicals is cyclooxygenase (COX)-2 and, therefore, inhibiting the activity of this enzyme is likely to reduce oxidative stress. In the present study an experimental rabbit model of hypercholesterolemia was developed and the effects of COX-2 inhibitors, nimesulide and celecoxib were observed on the activities of antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPx) and total antioxidant status (TAS). Rabbits were divided into four groups- control, saline, nimesulide and celecoxib, with all groups fed a high cholesterol diet, which only received saline. Low activities of SOD, GPx and TAS were measured in the hypercholesterolemic rabbits pretreated with saline. In the same group, a reciprocal relationship was observed between the LDL-cholesterol concentration and the plasma activities of GPx, SOD and TAS. Rabbits in nimesulide and celecoxib group showed significantly higher activities of SOD, GPx and TAS in hypercholesterolemic rabbits compared to saline group (p<0.05). Our study shows that selective and timely use of COX-2 inhibitors would be useful in preventing the onset and development of atherosclerosis by enhancing antioxidant defence system.
Highlights
Inflammation and oxidative stress are intimately involved in the pathogenesis of atherosclerosis [ ]
If this balance is perturbed in favour of more free radicals, either through an enhanced production or via a reduction in the endogenous antioxidant defence system or both, the body is at risk for free radical-mediated cell damage
First group was fed standard rabbit diet, second group was maintained on high cholesterol supplemented diet and pre-treated with saline, third group was maintained on high cholesterol supplemented diet and pretreated with nimesulide while fourth group was maintained on high cholesterol supplemented diet and pretreated with celecoxib
Summary
Inflammation and oxidative stress are intimately involved in the pathogenesis of atherosclerosis [ ]. The tissue concentration of oxygen radicals is limited under normal physiological conditions due to the existence of a delicate balance between the generation of free radicals and the antioxidant defense system [ ]. If this balance is perturbed in favour of more free radicals, either through an enhanced production or via a reduction in the endogenous antioxidant defence system or both, the body is at risk for free radical-mediated cell damage. The involvement of reactive oxygen species (ROS) in the oxidative modification of LDL is an important element of atherogenesis These ROS has drawn attention to the anti-oxidative defence of the organism, including the so-called ROS scavengers. Low TAS level is found in patients with atherosclerosis [ ], in cancer and rheumatoid arthritis
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