Modulation of cardiac and aortic peroxisome proliferator-activated receptor-gamma expression by oxidative stress in chronically glucose-fed rats.
ABSTRACT The aim of the present study was to examine the chronic effects of alpha-lipoic acid on proliferator peroxisome activated receptors-gamma (PPAR-gamma) and PPAR-alpha expressions in cardiovascular tissues of chronically hypertensive insulinoresistant rats. We have also evaluated the chronic effects of high levels of insulin, glucose, or both on superoxide anion (O(2)(-)) production in aortic smooth muscle cells (SMCs) in the presence or in absence of pioglitazone, a PPAR-gamma agonist.
The PPAR-gamma and PPAR-alpha expressions were measured by Western blot. The oxidative stress was evaluated by measuring the O(2)(-) production using the lucigenin method.
Increases in blood pressure, in aortic O(2)(-) production, in glucose or insulin levels, and in insulin resistance, as well as the decrease in PPAR-gamma protein levels in aorta and heart tissues were prevented or attenuated in glucose-treated rats fed with lipoic acid. Chronic treatment with pioglitazone prevented the marked increase in O(2)(-) production in cultured SMCs chronically treated with high insulin combined or not with high glucose levels.
The combined therapy with the antioxidant alpha-lipoic acid restored PPAR-gamma levels in cardiovascular tissues and attenuated or prevented the development of insulin resistance and hypertension in chronically glucose-fed rats. Moreover, the finding that pioglitazone was also efficient in preventing the increase in oxidative stress in SMCs treated with high insulin combined with high glucose concentrations supports the hypothesis that the activation of PPAR-gamma activity can counteract the oxidative stress that seems to be implicated in the development of hypertension and insulin resistance.
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ABSTRACT: ABSTRACT In the present study, the antioxidant activities of Hibiscus rosa-sinensis Linn. flower petals treatment for 4 weeks were screened in 10% D-glucose feeding in rats. Experimental rats were treated with 10% D-glucose solution to drink orally. H. rosa-sinensis flower petals (1,000 mg/kg of body weight) were mixed with normal chow diet and administrated for 4 weeks as preventive and curative effects. An appreciable decrease in peroxidation product viz. malondialdehyde is observed in heart tissues of H. rosa-sinensis treated in 10% D-glucose-fed rats. The decreased activities of key antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, and nonenzymatic antioxidants such as glutathione, vitamin E and vitamin C in 10% D-glucose-fed rats were brought back to near-normal range upon H. rosa-sinensis flower petals treatment. In conclusion, H. rosa-sinensis exhibited preventive and curative effects in 10% D-glucose-induced oxidative stress in rat heart tissues. PRACTICAL APPLICATIONS Acute oral glucose feeding causes oxidative stress and functional decline in heart of healthy subjects. Hibiscus rosa-sinensis is one of the medicinal plants that have attracted particular attention in folk medicine because of its widespread health use around the world. This study aims to enlighten the beneficial effects of H. rosa-sinensis in 10% glucose feeding-induced heart damage. These results led to development of a new phytomedicinal product with antioxidant activity to reduce heart diseases.Journal of Food Biochemistry 06/2011; 35(3). DOI:10.1111/j.1745-4514.2010.00417.x · 0.85 Impact Factor
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ABSTRACT: The aim of the present study was to examine the effects of acute infrasound exposure on oxidative damage and investigate the underlying mechanisms in rat cardiomyocytes. Neonatal rat cardiomyocytes were cultured and exposed to infrasound for several days. In the study, the expression of CAT, GPx, SOD1, and SOD2 and their activities in rat cardiomyocytes in infrasound exposure groups were significantly decreased compared to those in the various time controls, along with significantly higher levels of O2 (-) and H2O2. Decreased cardiac cell viability was not observed in various time controls. A significant reduction in cardiac cell viability was observed in the infrasound group compared to the control, while significantly increased cardiac cell viability was observed in the infrasound exposure and rosiglitazone pretreatment group. Compared to the control, rosiglitazone significantly upregulated CAT, GPx, SOD1, and SOD2 expression and their activities in rat cardiomyocytes exposed to infrasound, while the levels of O2 (-) or H2O2 were significantly decreased. A potential link between a significant downregulation of PPAR-γ expression in rat cardiomyocytes in the infrasound group was compared to the control and infrasound-induced oxidative stress. These findings indicate that infrasound can induce oxidative damage in rat cardiomyocytes by inactivating PPAR-γ.Cardiovascular toxicology 05/2013; 13(4). DOI:10.1007/s12012-013-9211-5 · 2.56 Impact FactorThis article is viewable in ResearchGate's enriched formatRG Format enables you to read in context with side-by-side figures, citations, and feedback from experts in your field.
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ABSTRACT: SIRT1 and PPARγ, host defenses regulating inflammation and metabolic functions, are suppressed under chronic high oxidant stress and inflammation (OS/Infl) conditions. In diabetes, dietary advanced glycation end products (dAGEs) cause OS/Infl and suppress SIRT1. Herein, we ask whether dAGEs also suppress host defense in adults without diabetes. The relationships between dAGEs and basal SIRT1 mRNA, PPARγ protein levels in mononuclear cells (MNC) and circulating inflammatory/metabolic markers were examined in 67 healthy adults aged >60 years and in 18 subjects, before and after random assignment to either a standard diet (regular >15 AGE Eq/day) or an isocaloric AGE-restricted diet (<10 AGE Eq/day) for 4 months. Also, the interactions of AGEs and anti-AGE receptor-1 (AGER1) with SIRT1 and PPARγ were assessed in wild type (WT) and AGER1-transduced (AGER1(+)) MNC-like THP-1 cells. We found that dAGE, but not caloric intake, correlated negatively with MNC SIRT1 mRNA levels and positively with circulating AGEs (sAGEs), OS/infl, MNC TNFα and RAGE. Basal MNC PPARγ protein was also lower in consumers of regular vs. AGE-restricted diet. AGE restriction restored MNC SIRT1 and PPARγ, and significantly decreased sAGEs, 8-isoprostanes, VCAM-1, MNC TNFα and RAGE. Model AGEs suppressed SIRT1 protein and activity, and PPARγ protein in WT, but not in AGER1(+) cells in vitro. In conclusion, chronic consumption of high-AGE diets depletes defenses such as SIRT1 and PPARγ, independent of calories, predisposing to OS/Infl and chronic metabolic disease. Restricted entry of oral AGEs may offer a disease-prevention alternative for healthy adults.Amino Acids 05/2013; DOI:10.1007/s00726-013-1502-4 · 3.65 Impact Factor