Background Diabetes is a downregulator of atrial natriuretic peptide (ANP), resulting in reduced nitric oxide level and low expression of endothelial nitric oxide synthase by which nitric oxide level get reduced. In the present study, we examined the role of ANP in reduced nitric oxide level, which may be responsible in controlling diabetic nephropathy in rats. Methods Serum nitrite/nitrate ratio, blood urea nitrogen, protein in urine, urinary output, serum creatinine, serum cholesterol, kidney weight, kidney hypertrophy, renal cortical collagen content, thiobarbituric acid level, and antioxidant enzymatic activities were assessed. Results Treatment with lisinopril (1 mg/kg) significantly attenuated diabetes-induced elevated glucose level, cholesterol level, and protein in urine concentration. Whereas ANP at low dose (5 μg/kg) has no effect on elevated markers of diabetic nephropathy, treatment with intermediate (10 μg/kg) and high-dose ANP (20 μg/kg) significantly attenuated the diabetes-induced increased blood urea nitrogen, protein in urine, urinary output, creatinine, cholesterol, kidney weight, kidney hypertrophy, renal collagen content, and thiobarbituric acid level and reduced endogenous antioxidant enzymatic activities. High dose of ANP was more effective in attenuating the diabetes-induced nephropathy, renal oxidative stress, and antioxidant enzyme activity as compared with the treatment with low-dose ANP (5 μg/kg), intermediate-dose ANP (10 μg/kg), or lisinopril (1 mg/kg, employed as standard agent). Administration of erythro-9-(2-hydroxy-3-nonyl)adenine, a phosphodiesterase-2 inhibitor (3 mg/kg), in combination with high-dose ANP significantly attenuated high-dose ANP induced ameliorative effects in diabetic nephropathy. Conclusions Taken together, these results indicate that diabetes-induced oxidative stress and lipid alterations may be responsible for the induction of nephropathy in diabetic rats. ANP at intermediate and high doses have prevented the development of diabetes-induced nephropathy by reducing the cholesterol level, protein in urine concentration, and renal oxidative stress and by increasing the nitrite/nitrate ratio, certainly providing the direct nephroprotective action.

No abstract

Epilepsy is a complex neurological disorder characterized by hypersecretion of excitatory neurotransmitters in the brain. Level ofantioxidant enzymes in the brain changes during seizure. There are many herbal supplements that posses antioxidant potential and might help inprevention and recovery of seizures when used as an adjunct with modern antiepileptic drugs. Objective: The present work was undertaken toevaluate the Ameliorative effect of Sodium valproate in combination with Juglans regia extract against Pentylenetetrazole (PTZ) inducedconvulsions in mice. Materials and Methods: Juglans regia ethanolic extract (JREE) were administered at doses of (200mg/kg and 400 mg/kgp.o) and Sodium Valproate (500mg/kg p.o.) one hour before the administration of PTZ (80mg/kg i.p.). Brain tissues were screened for MDA,Catalase, GSH and protein estimation. Result and Discussion: Administration of JREE in the low and high dose prolongs the onset of myoclonicjerks dose-dependently and also showed protection against PTZ-induced convulsions. PTZ induced seizures caused a significant increase in MDAlevels and a significant decrease in GSH and catalase levels in PTZ group as compared to the vehicle control group. Juglans regia pre-treatmentprevented the oxidative stress as indicated by significant decrease in MDA levels and significant increase in GSH and catalse levels incomparison to PTZ group. Conclusion: The present study showed ameliorative effect of combination of Sodium Valproate in anticonvulsantactivity of ethanolic extract of Juglans regia fruit against PTZ induced seizures and also its protective effect against seizure induced oxidativestress.

No abstract