The factor(s) which trigger the proliferation of liver cells after partial hepatectomy in rats are not yet known with certainty. A series of specific and/or non-specific substances are said to effect the proliferation of liver cells, but metabolic changes after partial hepatectomy possibly also act as a contributory causative factor in the stimulation of those substances. In order to define this question more clearly the changes in the serum concentrations of the following metabolites in the course of time after partial hepatectomy were determined: free fatty acids, cholesterol, triglycerides, glucose, free amino acids and total protein. A reduction in the serum concentrations of some fatty acids and of glucose, and an increase in that of the free amino acids, was observed shortly after partial hepatectomy. The increase in the plasma concentration of immunoreactive glucagon after partial hepatectomy is thus explained and appears not to be of decisive significance for the stimulation of liver cell proliferation after partial hepatectomy.

Amikacin (AK) has the largest spectrum of aminoglycosides. However, its use is constrained because of nephrotoxicity and ototoxicity. Ellagic acid (EA) is a polyphenol present in plants. It has antioxidant, anticarcinogenic, and antimutagenic characteristics. Cilostazol (CTZ) is a phosphodiesterase Ш inhibitor, it is a potent vasodilator and antiplatelet drug. CTZ has an inhibitory effect on reactive oxygen species and superoxide generation in addition to hydroxyl radicals scavenging action. This study determines whether EA and cilostazol have a protective effect against AK-induced nephrotoxicity. Forty-nine rats were divided into seven equal groups: control normal; AK 400 mg/kg; EA 10 mg/kg; CTZ 10 mg/kg; AK 400 mg/kg plus EA 10 mg/kg; AK 400 mg/kg plus CTZ 10 mg/kg; AK 400 mg/kg plus EA 10 mg/kg and CTZ 10 mg/kg. For seven days, drugs were administered using gavage one hour before intramuscular injection of AK. Twenty-four hours after the last AK dosage, blood samples were collected to determine blood urea nitrogen and creatinine levels. Kidneys were removed for histopathological examination and measurement of: malondialdehyde (MDA), catalase (CAT), decreased glutathione (GSH), superoxide dismutase (SOD), interleukin 6 (IL6), tumor necrosis factor-alpha (TNFα), nuclear factor kappa B (NFκB), and Bcl-2 associated x protein (BAX). AK caused kidney damage, inflammatory mediator elevation, and oxidative stress and apoptotic markers. Rats receiving EA or CTZ indicated significant improvement in kidney function, decrease in oxidative stress and inflammation through NF-kB down-regulation and BAX expression. The combination of EA and CTZ showed a synergistic effect. In conclusion, EA and CTZ might play a beneficial role in preventing nephrotoxicity induced by AK partially by inhibition of tissue inflammation and apoptosis.

Amikacin(AK) has the largest spectrum of aminoglycosides. However, its use is limited due to nephrotoxicity and ototoxicity. Ellagic acid (EA) is a plant phenolic structure. it has antioxidant, anticarcinogenic and antimutagenic properities. Cilostazol (CTZ) is a PDE Ш inhibitor, it is a potent vasodilator and antiplatelet drug. This study aimed to determine if EA and cilostazol have a protective effect against nephrotoxicity caused AK. Forty nine rats were divided into seven equal groups: control normal; AK 400mg/kg; EA 10 mg/kg; CTZ 10mg/kg; AK 400mg/kg plus EA 10mg/kg; AK 400mg/kg plus CTZ 10mg/kg; AK 400mg/kg plus EA 10mg/kg and CTZ 10mg/kg. For seven days, Drugs were given orally one hour before intramuscular injection of AK. After twenty-four hours from the last dosage, samples of blood were obtained to determine blood urea nitrogen (BUN) and creatinine levels in serum, kidneys were extracted and longitudinally divided into two parts, part for measuring the following parameters: malondialdehyde (MDA), catalase (CAT), reduced glutathione (GSH), interleukin 6 (IL6), superoxide dismutase (SOD), tumor necrosis factor-alpha (TNFα), nuclear factor kappa B (NFκB) and Bcl-2 associated x protein (Bax), the other part was placed in formaldehyde solution and examined under light microscopy for routine histopathologic examination. The results of the present study proved that EA, CTZ and their combination protected rats against AK - induced nephrotoxicity; This effect might be a result of the antioxidant, anti-inflammatory and anti-apoptotic properties of these compounds.

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