Effect of trapidil, an antiplatelet and vasodilator agent on gentamicin-induced nephrotoxicity in rats

Büyükafşar, Kansu; Yazar, Aziz; Düşmez, Duygu; Öztürk, Hakan; Polat, Gürbüz; Levent, Adnan

doi:10.1006/phrs.2001.0864

Cited by 33 publications

(19 citation statements)

References 24 publications

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“…This result is in the same line as the finding of Kurus et al 5 and may be due to the inhibition of endotheliumdependent vasodilatation. 38 The present results revealed that CsA induced a significant elevation in the level of superoxide anion and malondialdehyde (MDA) production and significantly reduced the activity of SOD, catalase, and reduced GSH. It is believed that reduced activity of one or more antioxidant systems because of the direct toxic effect of CsA causes an increase of lipid peroxidation and oxidative stress, and consequently renal and liver toxicity.…”

Section: Protective Effect Of Trapidil and L-arginine 965mentioning

confidence: 53%

Protective effect of trapidil andl-arginine against renal and hepatic toxicity induced by cyclosporine in rats

Salem

Maarouf

et al. 2010

Renal Failure

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(2010) Protective effect of trapidil and l-arginine against renal and hepatic toxicity induced by cyclosporine in rats, Renal Failure, 32:8,[959][960][961][962][963][964][965][966][967][968] DOI: 10.3109 CsA induced renal and hepatic dysfunction, which was confirmed by laboratory and histopathological examination. Administration of trapidil diminished the renal and liver injury and significantly attenuated the levels of serum creatinine, urea, aspartate aminotransferase (AST), alanine aminotransferase (ALT), interleukin1b (IL-1b), tumor necrosis factor alpha (TNF-a), monocyte chemoattractant protein-1 (MCP-1), and oxidative stress, while it significantly elevated the level of serum nitric oxide and the activity of antioxidative stress. L-Arginine gave the same trend as trapidil, but trapidil effect was more pronounced. Coadministration of trapidil + L-arginine significantly ameliorated the toxic effect of CsA, but did not differ significantly from the effect of trapidil alone. Conclusions: Treatment with trapidil or L-arginine diminished the renal and hepatic CsA-induced toxicity. However, the effect of trapidil was more pronounced. Therefore, treatment with trapidil alone may be the most economic and effective as a potential therapeutic agent in CsA injury.

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Section: Protective Effect Of Trapidil and L-arginine 965mentioning

confidence: 53%

Protective effect of trapidil andl-arginine against renal and hepatic toxicity induced by cyclosporine in rats

Salem

Maarouf

et al. 2010

Renal Failure

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“…This result may be due to the inhibition of endothelium-dependent vasodilatation. 56 NO with the heme moiety of soluble guanylyl cyclase leads to the formation of cGMP from GTP. 57 The toxic renal effects of GM observed in this study are manifested in significant elevation in MDA and superoxide anion production and significant reduction in GSH level and SOD, GSH-Px, and CAT activities.…”

Section: Discussionmentioning

confidence: 99%

Renoprotective Effect of Grape Seed Extract against Oxidative Stress Induced by Gentamicin and Hypercholesterolemia in Rats

Salem

2011

Renal Failure

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Rationale: Kidneys are dynamic organs and represent one of the major systems maintaining the body homeostasis; they are affected by many chemicals and drugs. Grape seed extract (GSE) has been targeted to prevent drug-induced renal toxicity. Objectives: This study investigates the possible renoprotective effect of GSE against oxidative stress, renal impairment, and hypercholesterolemia (HC) induced by gentamicin (GM) and cholesterol-enriched diet. Seventy adult male Wistar rats (160 ± 10 g) were divided into seven groups: (1) served as control, (2) GSE, (3) GM, (4) GSE + GM, (5) hypercholesterolemic (HC) group, (6) GM + HC group, and (7) GM + HC + GSE. Kidney functions, inflammatory mediators, cytokines, lipid profile, nitric oxide (NO), cyclic guanosine monophosphate (cGMP), and oxidative and antioxidative stress parameters were assessed in all groups. Main findings: GM induced renal dysfunction, which was exacerbated by the presence of HC as confirmed by laboratory determinations. Administration of GSE attenuated the renal toxicity evidenced in significant reduction in elevated kidney function, inflammatory cytokines as well as lipid profile, NO, cGMP, enzymatic, and nonenzymatic antioxidants. Conclusion: Administration of GSE simultaneously with GM attenuated oxidative stress, diminished renal toxicity, and improved lipid profile induced by GM and HC.

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“…A previous study demonstrated that gentamicin, an aminoglycoside antibiotic, decreased the glomerular filtration, and this reduction was reversed by co-administration of L -arginine [12]. Furthermore, trapidil, an antiplatelet and vasodilator agent which increased serum NO metabolites, attenuated gentamicin-induced renal failure [13]. Consequently, these findings indicate that gentamicin-evoked renal failure may involve the nitrergic system in the kidney.…”

Section: Introductionmentioning

confidence: 88%

Protective Effect of <i>L</i>-Arginine Intake on the Impaired Renal Vascular Responses in the Gentamicin-Treated Rats

Seçilmiş¹,

Karataş²,

Yorulmaz³

et al. 2005

Nephron Physiol

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The purpose of this study was to investigate the effect of gentamicin (100 mg/kg/day, i.p.) treatment on endothelium-dependent and -independent vasodilation in isolated perfused rat kidney, and the effect of amino acid L-arginine (in the drinking water, 2.25 g/l) on renal dysfunction induced by gentamicin. When gentamicin-treated groups were compared with the control group, it was observed that BUN and creatinine levels increased significantly. Also, the relaxant responses induced by acetylcholine, sodium nitroprusside and pinacidil decreased. Histopathological examination indicated acute tubular necrosis in this group. In animals treated with gentamicin together with L-arginine, there was a significant amelioration in the BUN and creatinine levels. The vasodilator responses were similar to those of the control group. Histopathological examination indicated only hydropic degeneration in tubular epithelium of kidney. Co-administration of L-N^G-nitroarginine methyl ester (L-NAME) (112.5 mg/l), an inhibitor of nitric oxide synthase, and L-arginine to rats treated with gentamicin did not change the protective effect of L-arginine. In rats receiving L-NAME alone, the level of BUN and creatinine and vasodilation to acetylcholine were not significantly different when compared to those of the control group, while relaxant responses to sodium nitroprusside and pinacidil were increased. These results suggest that gentamicin leads to an impairment in vascular smooth muscle relaxation in addition to acute tubular necrosis in the rat kidney. Supplementation of L-arginine has an important protective effect on gentamicin-induced nephropathy.

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Effect of trapidil, an antiplatelet and vasodilator agent on gentamicin-induced nephrotoxicity in rats

Cited by 33 publications

References 24 publications

Protective effect of trapidil andl-arginine against renal and hepatic toxicity induced by cyclosporine in rats

Protective effect of trapidil andl-arginine against renal and hepatic toxicity induced by cyclosporine in rats

Renoprotective Effect of Grape Seed Extract against Oxidative Stress Induced by Gentamicin and Hypercholesterolemia in Rats

Protective Effect of <i>L</i>-Arginine Intake on the Impaired Renal Vascular Responses in the Gentamicin-Treated Rats

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