| These years the study about the mechanism of liver injury and its prevention havebecame the the hot spot in biology and medical study in domestic and oversea. Aprotinin is akind of alkaline polypeptide,the inhibitor of unspecific serine proteinase.For clinical,theaprotinin is commonly used in arresting bleeding during surgery,pancreasinflammation,shock,asthma and gynecological illnesses etc.Aprotinin has protactive functionsin many experimental injuries such as bloodletting and blood re-get in liver,brain and heartinjuries has significant protection and there aren't any articals about that aprotinin has theprotective functions in acute liver injury and chornical liver fiberical. Right now,there aren'tany articals for the functions about aprotinin protecting the experimental mice'experimentalinjury and chornical liver fiberical,too. There were many studies about acute and chronic liverinjury they were only for the protection or therapeutic effects. But the articals for boththerapeutic effects and protection are very rare.This paper will use carbon tetrachloride to build the actue hepatic injury and chornic injuryfiberical mice models and use the aprotinin to protect mice liver.And will descuse its workingmechanism for the futher studying of protection of this illness and to find a effective method.This experiment will use ccl4 to build the experimental mice model and using aprotinin toprotect the mice liver. Results showed that compared the model control group and normalcomtrol group,the serum ALT and AST increased significantly ( p<0.001),the model controlgroup liver weight coefficent increased significantly ( p< 0.001) compared with the normalcontrol group.Compared the model control group and normal control group,,the liver malonicaldehyde content increased significantly.(p<0.001). The model control group liver tissue isturgid the centrol of the liver sub-phyllode showed spread and poly-incomplete necrosis andfat denaturation.The inflammation cells have been infiltrated.The mice acute hepatic injuryexperimential model was built very successfully. Compared the group, who had a lowerdosage, with the model control group we can see the serum ALT and AST decreasedsignificantly (p<0.01,P<0.05).Compared with the model control the liver weight coefficentdecreased,but it has no statistical meaning.It decreased the amount of the malonicaldehyde(p<0.01) of the hepatic injuried mices in liver tissue significantly.In the group withthe less amount of aprotinin the hepatic sub-phyllode spread turgided,the fat denaturated,theliver cells of the centrol part were necrosised. No inflammation cell infiltration was noticed.Itsfunction is the same with diammonium glycyrrhizinate injection group. Compared the mediumdosage aprotinin group with the model control group, the serum ALT and AST decreasedsignificantly(p<0.05/p<0.01). Compared with the model control group the liver weightcoefficent decreased significantly(p<0.05). Decreased the hepatic injuried mice'malonicaldehyde amount in the liver tissue. Compared with the model control group, the difference isvery significant(p<0.001).In the medium amount aprotinin group the periphery of the hepaticsub-phyllode, some of the liver cells had a little necrosis and fat denaturated,the degree of thenecrosis and the denaturation is less than the model control group.Its function is the same withdiammonium glycyrrhizinate injection group.Compared the maximum dosage of the aprotiningroup with the model control group,its serum ALT & AST decreasedsignificantly(p<0.001).Comparing with the model control group the liver weight coefficentdecreased significantly(p<0.01) Decreased the amount of the malonic aldehyde in the livertissue of the hepatic injuried mice.Compared with the model control group the difference isvery significant(p<0.001)In the maximum dosage group the liver sub-phyllode periphery fewliver cells are little turgid and little fat denaturated.Its function is better than the diammoniumglycyrrhizinate injection group.The results showed that aprotinin could protect the mice'liverfrom the acute liver injury significantly. This experiment used the ccl4 to build the chronic liver injury of experimential animalmodel by Wistar rats and gave aprotinin to protect the rats liver and to study the curingfunction.The results showed that compared the model control group with the normal controlgroup,its serum ALT and A/G decreased significantly,the serum SA decreased significantly theAKP increased significantly,the Hyd in the liver tissue increased significantly ,too.They all havestatistical meaning(p<0.001),the value of serum g-GT increased (p<0.05).The serum CHEdecreased,T-BIL increased,but they all have no statistical meaning.The model control grouphas the pathological changing,the hepatic fiber tissue proliferated significantly partitioned thehepatic sub-phyllode into two different sized fake phyllodes.In the fake phyllodes have nocentrol vein or the centrol vein inclined.The liver fat denaturated,in the cytosome there aremany different sized around vacuoles. There appeared something like heptocirrhosis.The ratschronic hepatic injury experimential animal model was built successfully.Compared the lessdosage aprotinin group with the model control group,the serum ALT and AST decreasedsignificantly(p<0.05),the value of ALB and A/G both increased(p<0.001),the value of SAincreased(p<0.01),the value ofCHEincreased(p<0.05),thevalueofg-GTdecreased(p<0.05).Comparedwith the model control group,the amount of the Hyd decreased,the value of T-BILdecreased,but has no statistical meaning. The less dosage aprotinin's pathological changing,the hepatic sub-phyllode structure was blurred.The liver cell chain isn't continual. Around themeeting section the liver cell denaturated seriously. In the hepatic cells there are manydifferent sized round vacuoles,some liver cells liquid denaturated very seriously,very few livercells are disintegrated and necrosised.Compared the medium dosage aprotinin group with themodel control group the serum ALT decreased significantly(p<0.05),the value of ALB and A/Gincreased(p<0.001,p<0.01),the value of SA increased(p<0.05).Compared with the model control group the ASTdecreased,thevalueofHyddecreased,thevalueofCHEincreased,the value of g-GT decreased, the value ofT-BIL decreased,but haven't very significant difference. The pathological changing of themedium dosage group: the structure of the hepatic phyllode is blurred,the centrol section ofthe hepatic sub-phyllode and some meeting section have medium fat denaturation,in the livercells there are many visible different sized around vacuoles.Compared the maximum dosageaprotinin group with the model control group the serum ALT decreased(p<0.05),the value ofthe ALB and A/G both increased(p<0.01),the value of CHE increased(p<0.05).Compared withthe model control group the AST decreased,the value of SA increased,the value of Hyddecreased,the value of g-GT decreased,the value of T-BIL decreased,but haven't anysignificant difference. The pathological changing of the maximum dosage aprotinin group:theliver has a little fat denaturation,in the liver there are many separated fat denaturation. Thepathological changes of the maximum dosage group is less than the hepatic cell growthhormone.The results showed that the aprotinin has both protective function for the chronicliver injury and curing function,it has very good antifiberical function. This experiment used ccl4 to build the acute liver injury animal model by Wistar rats,andused the take orally aprotinin to study its protective function.The results showed thatcompared the model control group with the normal blank control group,the serum ALT andAST both increased significantly(p<0.001),the serum NO increased significantly (p<0.01),GSH decreased significantly(p<0.01),compared the model control group with the normalblank control group the liver weight coefficent increased significantly(p<0.001).The liver cellsof the model control group turgided,the cytosome is loose,the centrol of the liver sub-phyllodebecame spread, poly-develop and incompleted necrosis and fat denaturation,the inflammationcell infiltrated significantly.The rats actue hepatic injury experimental model built successfully...
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