bicyclol and Kidney-Diseases

This study investigated the protective effects of bicyclol against cisplatin-induced nephrotoxicity and the possible mechanisms in mice. Bicyclol (250 mg/kg, p.o., 5 days) showed significant protection as evidenced by the decrease of elevated serum creatine and blood urea nitrogen, and improvement of histopathological injury induced by cisplatin. The formation of kidney malondialdehyde with a concomitant reduction of reduced glutathione were also inhibited by bicyclol, while the activities of kidney superoxide dismutase, catalase and glutathione peroxidase were all increased, respectively. Bicyclol also inhibited the increase of kidney and serum nitric oxide induced by cisplatin. In addition, induction of induced nitric oxide synthase and nitrotyrosine were suppressed by bicyclol. Bicyclol suppressed cisplatin-induced extracelluar signal regulated kinases 1/2 and p38 mitogen-activated protein kinase activation in the kidney of mice. Results obtained demonstrate that bicyclol pre-administration can prevent the nephrotoxicity induced by cisplatin.

Topics: Animals; Antineoplastic Agents; Biphenyl Compounds; Cisplatin; Disease Models, Animal; Free Radical Scavengers; Glutathione; Kidney; Kidney Diseases; Male; Malondialdehyde; Mice; Mice, Inbred ICR; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Mitogen-Activated Protein Kinase Kinases; Nitric Oxide; Oxidative Stress; p38 Mitogen-Activated Protein Kinases; Tyrosine

To investigate the protective effect of bicyclol on kidney injury induced by ischemia-reperfusion in rats.. Bicyclol was orally administered to rats at doses of 50 and 200 mg.kg-1 before ischemia-reperfusion injury to evaluate the influence of bicyclol on the formation of MDA and BUN in serum, the content of GSH and the activity of GST in kidney, as well as kidney mitochondria membrane fluidity in ischaemia-reperfusion rats.. Bicyclol given orally at doses of 50 and 200 mg.kg-1 was shown to significantly decrease the increment of MDA and BUN in serum and protect the GSH depletion in kidney. Bicyclol was also shown to induce kidney GST and ameliorate the decrease of mitochondria membrane fluidity. The protective effects of bicyclol on kidney injury induced by ischemia-reperfusion are dose-dependent.. The protective action of bicyclol on kidney injury induced by ischemia-reperfusion may be attributed to its induction of kidney GSH and the GST, stabilization on mitochondria membrane and the inhibition on lipid peroxidation.

Topics: Animals; Biphenyl Compounds; Blood Urea Nitrogen; Disease Models, Animal; Glutathione; Glutathione Transferase; Ischemia; Kidney Diseases; Male; Malondialdehyde; Membrane Fluidity; Mitochondria; Protective Agents; Rats; Reperfusion Injury