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

Abstract

(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.

Modulation of monosodium glutamate induced histological injuries, histomorphometrical alterations and DNA damage in the mice hepatic and renal tissues by oral administration Nano-cerium oxide and L-arginine and their combination

“…Likewise, treatment with L-Arginine caused moderate improvement in the histological alterations in hepatic and renal tissue induced by monosodium glutamate alone and significant improvement of DNA content. These were confirmed by work done by Elbassuonia et al, [33] , Salem et al [66] . The reported ameliorating effect of L-Arginine in the present study may be attributed to increasing of total antioxidant capacity, and antioxidant as renal SOD activity (A. Gupta,2007) [67] as well as decreasing ALT and AST levels (the hepatic injury markers), urea and creatinine (the renal injury markers) and oxidative stress through malonaldehyde decreasing [33] .…”

Calcium blockers inhibit cyclosporine A-induced hyperreactivity of vascular smooth muscle cells

“…In this case, the promoter for IL-2 is blocked (6,7). The application of CsA is associated with many side-effects, such as hypertension, renal failure, hepatotoxicity, neurological disorders or cancers, which cannot be eliminated to date (8). One of the main reasons for restricting the usage of CsA in certain situations is nephrotoxicity and hypertension in approximately 30% of patients.…”

Effect of Triazolopyridine (Trapidil) on Experimental Hepatorenal Toxicity Induced by Renal Ischemia Reperfusion Injury in Rats

“…Furthermore, it was proved that is trapidil inhibits leucocyte infiltration [41] and this proved by our results by significant decrease in tissue MPO in trapidil treated group as compared to I/R group also there is significant decrease in serum TNF-a , MCP-1 in trapidil treated group as compared to renal I/R group. Trapidil effect on MCP-1 expression may be attributed to its inhibitory effect on PDGF receptor, inhibition protein kinase A, and change in prostaglandin production [42] . Reduction in inflammatory cytokines may reduce tissue injury in hepatic and renal tissues and improves its function and inhibits more release of ROS [43] these results are supported by histopathological finding in our findings which reveals normal hepatocytes with slightly dilated central vein and blood sinusoids and normal renal glomeruli in group pretreated with trapidil before renal I/R.…”