| Background and PurposeThe history of alcohol consumption has been nearly as long as the history of mankind. Alcohol-related diseases represent a serious problem throughout the world and they show a gradually increasing tendency. It can be stated that the frequency of occurrence, severity and mortality of alcohol-related liver diseases(ALD) are in direct correlation with the amount of alcohol consumed. The direct hepatotoxic effect of alcohol and its metabolites has become obvious by now. Generally speaking, the rather wide spectrum of ALD includes alcoholic minimal(AML) % alcoholic fatty liver(AFL), alcoholic hepatitis(AH), alcoholic fibrosis(AF) and alcoholic cirrhosis(AC). AF can be regarded as a turning point in the pathological evaluation of ALD, because it can lead to cirrhosis - the irreversible stage of7AF that is considered to be one of the leading causes of morbidity and mortality. To effectively intervene or prevent this scarring process, we must first understand cellular and molecular mechanisms of liver fibrogenesis. For this reason, much attention has been focused on experiment models of AF. The present research was carried out to provide a relatively simple and feasible rat model for further elusive of the pathogenesis of AF. Twenty-seven rats were accepted daily tequila in doses of 7g/kg body weight for total 24 weeks to induce a rats model of AF. The serum biochemistry indices were monitored and the hepatic damages and fibrosis changes of chronic alcoholism were observed on weeks 4, 12 and 24 after the start of alcohol administration.Materials and MethodsThirty-three Sprague-Dawley rats, with weight of 180-210gm at the beginning of the experiment, were categorized into two groups. Twenty-seven rats were randomly assigned to receive 56%(v/v) ethanol calculated on a body weight basis, 7g/kg/d. Balanced diets were consumed ad libitum during the experiment. Six rats in control group were infused with the same diets as above except quantity of water instead of ethanol. Nine rats respectively in model groups were randomly sacrificed at 4th, 12th and 24th week after experiment, while the control rats were performed at the end of 24w. The animals were weighed weekly and at the terminal stage. After the rats were killed, the livers were removed, weighted, examined macroscopically and some were photographed. Serum proteins and enzymesconcentrations were measured including total protein (TP), albumin (AP), globulin (GP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP). Paraffin sections from the liver samples were stained with hematoxylin and eosin (HE) and Masson s trichrome( MT) method. The degree of steatosis and the activity of hepatitis were determined semi-quantitatively by a score fluctuating between 0 to 4 after HE staining, whereas fibrosis was assessed by SSS score system after MT method. HPIAS imaging analysis instrument was used to summarize the percentage of collagen area. The results of relative liver weight, laboratory tests and liver histology were compared between the two groups.ResultsThe rats in model groups presented nausea, diarrhea, slaver, sleep, loss of appetite, tardy behavior, poor luster of hair and slow weight gain in the early phase. These phenomena lightened as time being. After alcohol treatment, the livers were yellow-brown and felt fatty having a smooth capsular and cut surface. The hepatic relative weight of ethanol-fed rats gained compare with the controls, and was paralleled to inflammation and fibrosis in the liver.A marked down-regulation of serum protein levels was seen in the ethanol-fed animals; this was slightly more pronounced in 4w model group. It can be explained that acute impairment in the liver may lead to proteins insufficiency in serum. AST and ALP had evident elevate in 4w model group than that in healthy control rats ( median value was 218.83 v 152.00, P<0.05;265.33 v 71.83, P<0.01 ).Then AST fluctuated with the time of stimulation by ethanol, whereas ALP g...
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