| PrefaceAlcoholic liver disease(ALD),which is the most common cause of cirrhosis in the western countries caused by long-term alcohol intaked.ALD includes mild alcohol-induced liver injury,alcohol fatty liver,acute alcoholic hepatitis and alcoholic liver cirrhosis.ALD is divided into acute and chronic injury in China.if drinkers who continued drinking alcohol more than 40g/d and continued for more than five years can cause chronic liver injury,or if the consumption more than 80g/d and continued for more than two weeks can cause acute liver injury.The histological changes of the former include all the liver cells(include liver cell,stellate cell,liver sinusoidal endothelial cells.).cytokine(including PDGF,TNF-ALPHA),and extracellular matrix(MMP TIMP).Some of the mechanisms have already identifid.However,the stduy of the changes of histology in ALD is less,and AFL usually happen firstly.The relation of its formation with liver cell,cytokine,and extracellular matuix is not clear.And the study of effect of acute alcohol to liver sinusoidal endothelial cell and tight junction is less.In this study,through establishment of acute alcohol-induced liver injury of rats mode,we observed the changes of fenestrae of liver sinusoidal endothelial cells and tight junctions between liver cells.It will approach the mechanism of acute alcohol-induced liver injury advancedly. Methods1.Preparation of acute alcohol-induced hepatic injury modelRats were divided into two groups randomly:control,ethanol treatment,with 10 rats in each group.Gavages after fasting for 12 hours.Control group were received normal sodium(2.0ml)instead of ethanol.Ethanol-treated rats received ethanol[5g/kg body weight(BW)]by garage every 12 hours for a total of 3 doses.2.Histopathological examinationAt 4 hours after the last garage,the rats were anesthetized and subsequent a small sample of liver was fixed.Histopathological change was assessed by hematoxylin and eosin staining.Another fresh sample of liver tissue was fixed,dehydrated,and epoxy resin embedded with diamond thin knife into 50 nm,then double-acetic acid citrate oxygen uranium and double staining,by electron microscopic observation.Result1.The general condition of experimental animalThe rats in normal group acted actively,the reaction was normal.Two rats in the ethanol group acted slowly and reacted sluggishly after intragastric administration;one rat occurred piloerection,irritability,vesania,spasm,a fit of eleptiform at times.Three rats in the alcohol group died in the process of making-mode.2.Histopathological changesIn the control group,the construction of liver is complete,and cell chord arrange in radical order with the central of central veins.The edge of acini hepatic sharpness. Liver cells is polygon,and demarcation is clear,nuclears is round and clear,located in the middle of the cells,cytoplasm is profusion.In the ethanol group,the sinus hepaticus expanded,liver cellulars swelled, cytoplasm rarefacted and can find amount of inequality size of leipo-vacuolus,liver cells acidophily changed,small amounts of phlegmonosis infiltrated in lobula central veins and converge vessel domain. 3.The changes of liver histopathology in electron microscopeIn the control group the endothelial cell have many inequality size of fenestrae, which have no diaphragrna,intracytoplasm have ponds of pinocytosis bullules.Intercellular is large,and have no subepithelial membrane under the endodermis.In ethanol group liver sinusoidal endothelial cells hyperplasy slightly,and quantity of fenestraes reduced,diameter increased.Two of the fenestraes even appear to break.The number of tight junctions between liver cells reduced,cloudiness,layer changed,break,and stiffness in acute alcohol-induced liver injury.Conclusion1.In acute ethanol-induced liver injury model of rats,liver sinusoidal endothelial cells hyperplasy slightly,and quantity of fenestraes reduced,diameter increased.Some of the fenestraes even appeared to break.2.The number of tight junction between liver cells reduced,became cloudy,and layer changed,break,and became stiffness in acute ethanol-induced liver injury model. |
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