Effects of captopril and losartan on lipid peroxidation, protein oxidation and nitric oxide release in diabetic rat kidney

Modification of cardiac oxidative stress in alloxan-induced diabetic rabbits with repaglinide treatment

“…This increase may be due to the poor antioxidant capacity as a consequence of low GSH and AA levels. These results are in accordance with some previous studies concerning diabetic tissues (Bhor et al, 2004;Gumieniczek, 2005;Yawuz et al, 2003).…”

Effect of diabetes on aortic nitric oxide synthesis in spontaneously hypertensive rats; does captopril modulate this effect?

“…Angiotensin converting enzyme (ACE) inhibitors, because of their protective effects for the cardiovascular system and kidney, are regarded as first-line antihypertensive drugs for patients with diabetes (World Health Organization, 1999). Mechanisms that account for the protective effects of ACE inhibitors on diabetesinduced vascular dysfunction are not fully known, but they are probably related to increased insulin sensitivity (Torlone et al, 1993), inhibition of oxidative stress (Yayuz et al, 2003), and modulation of the NO pathway (Rajagoplan and Harrison, 1996). In the present investigation, we report the effect of diabetes on aortic NO in SHR and the possible modulation of this effect by the administration of captopril.…”

Effects of Ginkgo biloba on prevention of development of experimental diabetic nephropathy in rats

“…To evaluate the effects of GbE on DN, in our present work we used captopril (CAP) as an antifibrotic control drug [9,10] , and studied the possible influences of GbE on the parameters that indicate protective effects against the progress of DN, such as blood glucose, AGE, TGF-β1, MMP-2, TIMP-2, CTGF, collagen IV and laminin in the kidney cortex, anti-oxidases in the serum, and the thickness of the glomerular base membrane (GBM) on early experimental DN rats, and observed the morphological changes on DN rats. Induction of DN model and study protocol Diabetes mellitus was induced in the male Sprague-Dawley rats, by ip injection of 60 mg/kg of the beta-cell toxin STZ (dissolved in pH 4.5 citrate buffer immediately before the injection), while controlled normal standard rats (NS group, n=13) received 6 mL/kg citrate buffer.…”