Amelioration of chronic cyclosporine A-induced nephrotoxicity by telmisartan in rats

Al-Amran, Fadhil G.; Hadi, Najah R.; Kamoona, Talib H.; Kadhum, Zahraa J.

doi:10.5897/ajpp11.005

Cited by 5 publications

(2 citation statements)

References 35 publications

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“…In the present study, it has been observed that GSH decreased with increasing dosage in renal recipients which compatible with Mostafavi-Pour et al, (41) who documented that decreased in GSH levels in CsA treated patients suggested a possible direct interference of the drug with the intracellular homeostasis of glutathione (42) . Other study in rats showed that CsA had an effect on lipid peroxidation; it caused significant decrease in the antioxidant status that are GSH and catalase enzyme activity (43) .…”

Section: Discussionmentioning

confidence: 90%

Effect of Cyclosporine on the Relevant Biochemical Parameters in Renal Transplantation Patients in Mosul/Iraq

Alkass¹,

Yousif²,

Hamid³

et al. 2013

J.Edu.Sci.

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Section: Discussionmentioning

confidence: 90%

Effect of Cyclosporine on the Relevant Biochemical Parameters in Renal Transplantation Patients in Mosul/Iraq

Alkass¹,

Yousif²,

Hamid³

et al. 2013

J.Edu.Sci.

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“…For tubular injury: 0 = no tubular injury; 0.5 = <5% of tubules injured; 1 = 5–20%; 1.5 = 21–35%; 2 = 36–50%; 2.5 = 51–65%; and 3 = >65% of tubules injured. 29…”

Section: Methodsmentioning

confidence: 99%

Allicin ameliorates kidney function and urinary bladder sensitivity in cyclosporine A-treated rats

et al. 2016

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Cyclosporine-A (CsA) is an immunosuppressive drug which has been used to prevent rejection after organ transplantation and to treat certain autoimmune diseases. However, its therapeutic use is limited by nephrotoxicity. In this study, the modulator effect of allicin on the oxidative nephrotoxicity of CsA in rats was investigated. Furthermore, the effect of allicin on CsA-induced hypersensitivity of urinary bladder rings to acetylcholine (ACh) was estimated. Rats were divided into three groups, control, CsA (15 mg/kg, subcutaneously), and CsA/allicin (50 mg/kg, orally). At the end of the study, all rats were killed and then blood, urine samples, and kidneys were taken. CsA administration caused a severe nephrotoxicity which was evidenced by elevated kidney/body weight ratio, serum creatinine (Cr), blood urea nitrogen, lactate dehydrogenase, and urinary protein with a concomitant reduction in serum albumin and Cr clearance as compared with control. A significant increase in renal contents of malondialdehyde, myeloperoxidase, and tumor necrosis factor-alpha with a significant decrease in renal reduced glutathione, superoxide dismutase activities, and nitric oxide (NOx) content was detected upon CsA administration. Exposure to CsA increased the sensitivity of isolated urinary bladder rings to ACh. Histological analysis revealed that CsA caused tubular necrosis and moderate diffuse tubular atrophy. Allicin protected kidney tissue against the oxidative damage and the nephrotoxic effect of CsA and significantly reduced the responses of isolated bladder rings to ACh. Our study indicates that allicin administration has the potential to protect against CsA-induced renal injury by reducing oxidative stress and inflammation and restoring NOx level.

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Angiotensin II type 1 receptor antagonists in animal models of vascular, cardiac, metabolic and renal disease

Michel

Brunner

Foster

et al. 2016

Pharmacology & Therapeutics

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We have reviewed the effects of angiotensin II type 1 receptor antagonists (ARBs) in various animal models of hypertension, atherosclerosis, cardiac function, hypertrophy and fibrosis, glucose and lipid metabolism, and renal function and morphology. Those of azilsartan and telmisartan have been included comprehensively whereas those of other ARBs have been included systematically but without intention of completeness. ARBs as a class lower blood pressure in established hypertension and prevent hypertension development in all applicable animal models except those with a markedly suppressed renin-angiotensin system; blood pressure lowering even persists for a considerable time after discontinuation of treatment. This translates into a reduced mortality, particularly in models exhibiting marked hypertension. The retrieved data on vascular, cardiac and renal function and morphology as well as on glucose and lipid metabolism are discussed to address three main questions: 1. Can ARB effects on blood vessels, heart, kidney and metabolic function be explained by blood pressure lowering alone or are they additionally directly related to blockade of the renin-angiotensin system? 2. Are they shared by other inhibitors of the renin-angiotensin system, e.g. angiotensin converting enzyme inhibitors? 3. Are some effects specific for one or more compounds within the ARB class? Taken together these data profile ARBs as a drug class with unique properties that have beneficial effects far beyond those on blood pressure reduction and, in some cases distinct from those of angiotensin converting enzyme inhibitors. The clinical relevance of angiotensin receptor-independent effects of some ARBs remains to be determined.

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Amelioration of chronic cyclosporine A-induced nephrotoxicity by telmisartan in rats

Cited by 5 publications

References 35 publications

Effect of Cyclosporine on the Relevant Biochemical Parameters in Renal Transplantation Patients in Mosul/Iraq

Effect of Cyclosporine on the Relevant Biochemical Parameters in Renal Transplantation Patients in Mosul/Iraq

Allicin ameliorates kidney function and urinary bladder sensitivity in cyclosporine A-treated rats

Angiotensin II type 1 receptor antagonists in animal models of vascular, cardiac, metabolic and renal disease

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