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1.
Egyptian Journal of Histology [The]. 2009; 32 (2): 333-345
em Inglês | IMEMR | ID: emr-136360

RESUMO

L-arginine, a semi essential amino acid, is the main source for the generation of nitric oxide via nitric oxide synthase. Nitric oxide plays a crucial role in the pathogenesis of acute renal failure. This study aimed to investigate if L-Arginine has a protective role in glycerol induced renal failure in rats. Forty adult male albino rats were randomly allocated into four equal groups. Group I [Control 1]: The rats were intramuscularly injected with a single dose of saline solution. Group II [Control 2]: L-arginine was once given through nasal gastric tube [125 mg/kg body weight]. Group Ill: Acute renal failure was induced by single intramuscular injection of 50% glycerol [10 ml/kg body weight]. Group IV: L-arginine was given as in group II an hour before glycerol which was injected similarly to group III. Eighteen hours after the end of treatment in each group, blood samples were extracted for estimation of renal functions. Kidneys were removed and used for light and transmission electron microscopical studies. For light microscopic purpose, paraffin sections were stained with Hematoxylin and Eosin, Periodic Acid Schiff and immunohistochemically for tissue inducible nitric oxide. Using image analyzer, quantitative measurements and analysis of the optical densities for Periodic Acid Schiff and inducible nitric oxide positive reactions were done. One-way ANOVA followed by Dunnett's test and Chi square test were used to determine the significance between the groups. Glycerol in group III led to deterioration of renal functions; degeneration, necrosis, sloughed brush borders, increased inducible nitric oxide staining density, dense nuclei and small atrophic mitochondria of the proximal convoluted tubules, thickness of foot processes, distorted and thickened glomerular basal lamina, as well as swollen glomerular capillaries endothelial cells with electron dense deposition. These changes were markedly reduced by using L-arginine in group IV. The findings implied that L-arginine plays an important role in protection against glycerol induced acute renal failure

2.
Egyptian Journal of Histology [The]. 2009; 32 (2): 417-430
em Inglês | IMEMR | ID: emr-136368

RESUMO

Thioacetamide induces liver injury, with histological alterations similar to those observed in human cirrhosis, through releasing of tumour necrotising factor-alpha. Pentoxifylline is an anti-tumour necrotising factor-alpha which might decrease the hepatic injury. This study investigated the histological and imniunohistochemical basis for the postulated beneficial role of pentoxifylline on the thioacetamide induced liver injury. Fifty adult male albino rats were divided into 5 equal groups; group I [Control 1]: Rats were intraperitoneally injected once daily with distilled water for 8 days; group II [Control 2]: Rats were intraperitoneally injected with pentoxifylline [200 mg/kg body wt] once daily for 8 days; group III [Liver injury induced group]: Rats were intraperitoneally injected with thioacetamide [50 mg/kg] once daily for 8 days; group IV [Preventive group]: rats were concomitantly intraperitoncally injected with pentoxifylline and thioacetamide in doses and duration similar to groups II and III, respectively; group V [Therapeutic group]: Rats were injected with thioacetamide for 8 days as in group III and then injected with pentoxifylline from day 9 to day 16 in similar doses as in group II. Blood samples were collected for estimation of liver enzymes. Liver was removed and used for light and transmission electron microscopical studies. For light microscopic study, the paraffin sections were stained with Haematoxylin and Eosin, Periodic Acid Schiff, Azan stain and immunohistochemically for tissue tumour necrotising factor-alpha. Using image analyzer, quantitative measurements and analysis of the optical densities for the Periodic Acid Schiff, Azan and tumour necrotising factor-alpha positive reactions were done. One-way ANOVA followed by Dunnett's test and Pearson's correlation coefficient [r] were used. Thioacetamide [Group III] led to elevated liver enzymes. Light microscopical study revealed degeneration and necrosis of hepatocytes, reduced glycogen, increased collagen and increased expression of tumour necrotising factor-alpha in the liver tissue. Electron microscopic study revealed degeneration of the cellular organelles. These changes were attenuated by using the pentoxifylline in preventive and to some extent in therapeutic groups. Thioacetamide induced hepatic injury can be prevented and treated by using pentoxifylline

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