Relation between resistin, PPAR-γ, obesity and atherosclerosis in male albino rats.

Obesity and atherosclerosis are inflammatory states involving variable metabolic signals. The adipokine resistin is implicated in adipose tissue dysfunction and is modulated by PPARγ. In this study, resistin and PPARγ role is investigated in the development of CVS disease. Forty-eight Adult male albino rats were divided into control, obesity and atherosclerotic groups; each group is divided into two subgroups; with and without PPARγ agonist administration for 8 weeks. To assess pathological changes; lipid profile, inflammatory mediator, serum resistin level and resistin expression in adipose tissue were measured. Aorta is histopathologically evaluated. It was found that resistin expression is significantly correlated with lipid profile and inflammatory status in obesity and atherosclerotic groups, and PPARγ agonist administration significantly improves inflammatory status and dyslipidemic profile across studied groups (p < .05). Aortic wall shows histopathological evidence of atherosclerosis in obesity group which is more evident in atherosclerotic group, and milder changes upon receiving PPARγ agonist.

Protective effect of apelin preconditioning in a rat model of hepatic ischemia reperfusion injury; possible interaction between the apelin/APJ system, Ang II/AT1R system and eNOS.

Introduction: Hepatic ischemic reperfusion injury occurs in multiple clinical settings. Novel potential protective agents are still needed to attenuate this injury. Apelin preconditioning protects against ischemic reperfusion injury in different organs. However, the protective mechanism of apelin on hepatic ischemic reperfusion injury is not yet clear. Aim: Evaluate the effect of apelin-13 preconditioning on hepatic ischemic reperfusion injury and clarify possible interactions between apelinergic, renin-angiotensin systems and endothelial nitric oxide synthase. Methods: In total, 60 rats were assigned to four groups: control sham-operated, ischemic reperfusion, apelin-treated ischemic reperfusion and apelin + N-nitro-L-arginine methyl ester-treated ischemic reperfusion. Apelin 2 µg/kg/day and N-nitro-L-arginine methyl ester 10 mg/kg/day were injected intraperitoneally daily for 3 days and 2 weeks respectively before hepatic ischemic reperfusion. Serum aminotransferase, aspartate aminotransferase, hepatic malondialdehyde, apelin, gene expression of caspase-3, endothelial nitric oxide synthase and angiotensin type 1 receptor and liver histopathology were compared between groups. Results: Apelin significantly reduced serum aminotransferase, aspartate aminotransferase, hepatic malondialdehyde, caspase-3 and angiotensin type 1 receptor expression, whereas hepatic apelin and endothelial nitric oxide synthase expression were significantly increased with improved hepatic histopathology. N-nitro-L-arginine methyl ester co-administration partially reversed this hepatoprotective effect. Conclusion: Apelin-13 reduced hepatic ischemic reperfusion injury. This protection could be related to the suppression of hepatic angiotensin type 1 receptor expression and elevation of hepatic apelin level and endothelial nitric oxide synthase expression, which counteracts the pathologic effects of Ang II/angiotensin type 1 receptor. An interaction exists between apelinergic, renin-angiotensin systems and endothelial nitric oxide synthase in hepatic ischemic reperfusion pathophysiology.