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egulation of oxidative stress. Teissier et al. (2004) has reported that the administration
of synthetic pPAR agonists to isolated macrophages has caused the activation of
NADpH oxidase which is one of the key enz¡imes involved in the intracellular production
of oxygen free radicals (Teissier et al. 2004). This study has also shown that the PPAR
agonist-induced activation of NADPH is mediated by the activation of PPAR-o (Teissier
et al. 2004). The usage of PPAR o agonists was also found to be beneficial in the
prevention of oxidative stress-induced hepatic fibrosis in thioacetamide (TAA) rat
cirrhosis model (Toyama et al. 2004). Toyama T et al. ( 2004) has reported that the
activation of PPAR û, was able to attenuate the TAA-induced depression of catalase in
liver tissue thus preventing the increase in oxidative stress induced damage and resulting
in the absence of hepatic fibrosis (Toyama et al.2004). A study by Villegas et al. (2004)
has shown that the pretreatment with rosiglitazone, PPAR y agonist, in rat gastricischemia-reperfusion
model was able to prevent the development of free radical-induced
damage (Villegas et al. 2004). This study has also reported that pretreatment with
rosiglitazone has resulted in the decrease in cytokine levels such as TNF-a in gastric
tissue and was accompanied by the decrease in the activity of xanthine oxidase and
superoxide dismutase (Villegas et al. 2004). PPAR y agonists are also found to protect
against oxidative stress induced vascular damage in rabbit model of hypercholesterolemia
(Tao et al. 2003). The antioxidant properties of PPAR B/ô and PPAR cr still remain to be
explored.
v.e.The role of PPAIÌ receptors in the cardiovascular sYstem
Due to the fact that variety of metabolic functions are regulated by the action of
PPAR receptors these receptors may play a significant role in the number of
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