Protective effect of Phyllanthus niruri against cyclosporine A-induced nephrotoxicity in rats

Kanchana, Karvannan; Parameswari, C. S.

doi:10.1007/s00580-012-1493-7

Cited by 2 publications

(3 citation statements)

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“…Moreover, interstitial nephritis and shrunken glomerular tufts were observed. Also in agreement with Kanchana and Parameswari (2013) reported that there were marked necrosis and dilatation of proximal tubules with tubular cell desquamation and massive infiltration with inflammatory cells after cyclosporine administration. Cid et al (2003) also reported loss of proximal tubular cells brush border with dilatation, necrosis, and infiltration of white blood cells in the tubules of renal cortex.…”

Section: Discussionsupporting

confidence: 91%

“…Liu and Tan (2020) stated that cyclosporin A caused an increase in serum urea and createinine levels, and decrease in their clearance levels as compared to the control group Kanchana and Parameswari (2013) reported that oral administration of cyclosporine by a dose of 25 mg/kg for 21 days was associated with significant elevation in the circulating levels of blood urea nitrogen and serum creatinine. These results were in agreement with the results recorded by Farag et al (2015) and Haleagrahra et al (2009) who stated that in CsA-treated rats, serum creatinine and urea levels were significantly increased compared to control rats.…”

Section: Discussionmentioning

confidence: 99%

“…In conditions of oxidative stress the cell induce several enzymatic and non-enzymatic systems to counteract the ROS and other free radicals but they are insufficient (Kanchana & Parameswari, 2013).…”

Section: Discussionmentioning

confidence: 99%

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Experimental study of renal toxicity of cyclosporine and the ameliorative effect of N-acetylecysteine in albino rat

Abdelkader

Hilal

Torky

et al. 2021

Ain Shams Journal of Forensic Medicine and Clinical Toxicology

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Introduction: Cyclosporine A (CsA) is considered powerful immunosuppressive drug which has improved the quality of life and survival rate of transplant patients and also used in autoimmune diseases. However, its use is limited by many side effects mainly nephrotoxicity. NAC is an antioxidant found to reduce CsA toxicity. Aim of the work: The study aims to determine the effect of exposure to cyclosporine on the kidney and to investigate the protective role of NAC. Methods: the study conducted on 50 adult male albino rats for 4 weeks, divided into 5 groups, group A the negative control group, group B the olive oil group (0.5 ml/d orally), group C the cyclosporine group (25mg/kg/d orally), group D the NAC group (600mg/kg/d orally) and group E the cyclosporine+NAC group. At the end of the study the evaluation was done by biochemical analysis and histopathology. Results: cyclosporine significantly affects the kidney by morphological changes in the form of dilatation of urinary space with congestion and lobulation of glomerullar capillaries in the renal corpusle. Proximal convoluted tubules showed degeneration of their cells with irregularity and destruction of brush border. Degeneration of distal convoluted tubules with exfoliation of some cells inside the lumen and the peritubular capillaries were congested and extravasated. Also cyclosporine affects the kidney by increasing serum urea and creatinine levels, while coadministration of NAC with cyclosporine attenuate its effects. Conclusion: cyclosporine causes renal injury through oxidative stress and NAC as an antioxidant attenuates but not fully protect against cyclosporine induced injuries.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%