N-acetylcysteine attenuates cyclosporine-induced nephrotoxicity in male albino rats

Cyclosporine A [Cs A] is used for the treatment of autoimmune and inflammatory disorders. However, Cs A-induced nephrotoxicity remains an important clinical problem, and oxidative stress has been implicated as a possible responsible mechanism. We assessed the protective ability of N-acetylcysteine [NAC], an antioxidant, against Cs A-induced nephrotoxicity. Thirty adult male albino rats were used to study the effect of cyclosporine [Cs A] and the action of N-acetylcysteine [NAC] on certain renal parameters; Blood Urea Nitrogen [BUN] and creatinine. Malondialdehyde [MDA] and catalase [CAT] levels were used as biomarker for testing the antioxidant potential of the drug. Endothelin-l[ET-l] levels were estimated in plasma. Animals were randomly assigned into three groups. Group I rats as control, group 2 were treated with Cs A and group 3 with Cs A plus NAC. Cs A administration for 21 days produced elevated levels of MDA and decreased in antioxidant enzyme CAT and deteriorated the renal function as assessed by increased serum Blood Urea Nitrogen [BUN] and creatinine. Plasma ET-l was also elevated as compared to control groups. Oral administration of NAC [140 mg/kg/day] significantly attenuated renal dysfunction, reduced elevated levels of MDA, increased the level of CAT and decreased level of ET- 1. These results indicate that NAC produces a protective mechanism against Cs A-induced nephrotoxicity in rats and suggest a role of Cs A for oxidative stress and the nephroprotective role of NAC against Cs A-induced nephrotoxicity in rats

Studying the effect of L-ascorbic acid on oral hypoglycemic drug [gliclazid] in treatment of diabetic albino rats

In this work, thirty adult male albino rats were used to study the effect of L - ascorbic acid on oral hypoglycemic drug [gliclazid] in treatment of diabetic rats. Rats were divided into three equal groups, I, II, III. Rats subjected to induction of diabetes by alloxan 100 mg /kg body weight. Rats showing fasting blood glucose level above 150 mg/dl were selected for the study. Group I received gliclazid 7 mg/Kg body weight Group II received gliclazid 7 mg/kg + L .ascorbic acid [L .A .A] 40 mg/Kg body weight. Group III received gliclazid 7 mg/kg + L .A .A 60 mg/kg body weight. Blood glucose level determined at different time interval after administration of drugs. The study showed that L.A.A produced hypoglycemic effect in a dose dependent manner in diabetic rats. Also, L.A.A/gliclazid produced early onset of action and maintained for long period compared to gliclazid treatment only

Marked suppression of experimental autoimmune myocarditis by simvastatin therapy in adult male wistar rats

Experimental autoimmune myocarditis [EAM] is a well-established animal model for human autoimmune myocarditis and postmyocardilis dilated cardiomyopathv. Recently, independent of their anti-hyperlipidemic properties, statins have been categorized as new agents that ameliorate the course of several organspecific autoimmune inflammatory diseases. Thus, this study aimed to assess the possible immunoinflammatory suppressive potentiality of simvastatin therapy on EAM. Three groups of male Wistar rats were investigated in this study: Normal control group, untreated-EAM and simvastatin- treated EAM, EAM was induced by subcutaneous immunization with porcine cardiac myosin at days, 0 and 7. Simvastatin [10 mg/kg per day] was administered orally for 20 days. On day 21, the hearts were dissected out, weighed, and prepared for histological and immunohistochemical examinations. To evaluate the effects of simvastatin therapy on production of T helper type-1 [Th1], proinflammatory cytokines: tumor necrosis factor- alpha [TNF-alpha] and interferon- gamma [IFN-gamma], and the plasma cholesterol levels were measured at days 11 and 21 in all groups. Daily administration of simvastatin to rats with EAM efficiently suppressed myocarditis development, its histopathological severity, and macrophages infiltration [ED1+ Cells] and other mononuclear cells into hearts. The treated rats had significantly decreased heart weight and heart weight/body weight ratio [Hw/Bw] compared with untreated animals. The up-regulated serum levels of TNF-alpha and IFN gamma during the course of EAM were promptly down-regulated by simvastatin therapy. Plasma cholesterol levels did not differ between the groups. Our data reveal that chronic therapy with simvastatin potentially ameliorated EAM via inhibition of Th1 proinflammatory cytokine production and macrophage infiltration, and this activity is independent on cholesterol reduction. Furthermore, we anticipate that simvastatin could be a new immunotherdpeutic tool for autoimmune myocarditis and other cardiac autoimmune impairments

Effect of chromium deficiency and supplementation on some aspects of carbohydrate and lipid metabolism in male albino rats

In this work, thirty adult male albino rats were used to study the effect of chromium deficiency and supplementation on carbohydrates and lipid metabolism. Rats were divided into three equal groups control, chromium deficient and chromium supplemented. Rats of the first group were fed on normal diet, rats of the second group were fed on a chromium deficient diet. Rats of the third group were fed on the same chromium deficient diet but were supplemented with oral chromium picolinate [90 |-l micro gm / kg body weight] daily for forty five days. At the end of the experimental period [45 days] plasma glucose, insulin serum triglycerides, cholesterol, LDL and HDL were determined. The study showed that chromium deficiency led to a significant increase in plasma glucose level, and insulin with insignificant changes in serum triglycerides, cholesterol, HDL and LDL as compared to control group. The study showed also that chromium supplementation led to an insignificant increase in serum glucose and insulin with significant decrease in serum triglycerides, cholesterol, LDL and a significant increase in serum HDL