Influence Of Polysaccharide From Compound Qiling Medicament On Chemical Acute Liver Injury In Chicken

The objective of the present study was to investigate the role of conservation andrestoration of the Qiling polysaccharide on the chemical acute liver injury caused bythe carbon tetrachloride to explore the action mechanism of Qiling polysaccharide.Meanwhile, study the relationship between N-acetyl-β-D-glucosaminidase（NAGase）and chemical acute liver injury.This experiment used the Ultrasonic Assisted and the Anthrone-sulphoacidMethod to extract the qiling san polysaccharide and to determine the content and theyield rate of the Qiling polysaccharide. The result shows the content of polysaccharideis39.71%.In this experiment,96chickens that were fifteen day old were divided into onecontrol group and five experimental groups with16each. Chickens in experimentalgroups were given Carbon tetrachloride-peanut oil solution with8,12,14,16,18mL·kg^-1respectively,by gavage.Four chickens in each group were killed aftergavaging12h,24h,48h,72h respectively. Blood and tissue organs were taken topathological examination. By detecting the activity changes of the Alanine AminoTransfer Enzyme （ALT） and Aspartate Aminotransferase （AST） in serum, andobserving the histopathological changes of the liver to establish the experimentalanimal models of chicken liver damage. The results indicated that the serum activityof ALT, AST to12mL·kg^-1dose increased significantly higher than any other groups,furthermore, peaked at48h.In this experiment,96chickens that were all one day age were randomly dividedinto two treatment groups, marked E and F. Both E group and F group were dividedinto six groups with blank control group, challenge by carbon tetrachloride group,biphenyl ester positive control group and three Qiling polysaccharide groupscontaining150mg·kg^-1、300mg·kg^-1、600mg·kg^-1. The blank control group wasrearing isolation, and except the blank control group and challenge group, each groupwas gavaged with corresponding drug from day8. Group E was gavaged for twoweeks and the F group was gavaged for four weeks.The challenge group and the three Qiling polysaccharide groups were gavage with Carbon tetrachloride-peanut oilsolution to modeling in the first day、fourth day and seven day of the second feedingweek on the concentration of12mL·kg^-1polysaccharide. After48h from the lasttime modeling, chickens of E group were killed, and the F group was after two weeksfrom the last time modeling.By determining the changes of alanine aminotransferase, aspartate aminotransfera-se,total bilirubin,N-acetyl-β-D-glucosaminidase,liver malondialdehyde and reducedglutathione in the serum, and observing the microstructure of liver tissue to systematicstudy the effect of Qiling polysaccharide to the chickling liver injury caused bycarbon tetrachloride and the correlation between N-acetyl-β-D-glucosaminidase andchicken acute liver injury.The results are as follows.E group:（1）After we fed chicken polysaccharide two weeks, compared with thecontrol group, chicken liver gain most weight in model group; in low-dose group,middle-dose group and high-dose group, the chicken liver index were highlysignificant difference （P<0.01）. Compared with the model group, the liver index ofeach group were tested different or significantly reduced （P<0.05or0.01）. Comparedwith the positive group, low-dose group, middle-dose group and high-dose group, thechicken liver index difference was not significant （P>0.05）.（2）Orally polysaccharidetwo weeks CCl₄acute liver injury induced chicks serum ALT, the AST activity TBiLcontent changes in comparison with the control group, model group was significantly（P<0.01）. Compared with model group, low-dose group, middle-dose group, and highdose polysaccharide group and positive group can be very significantly reduced CCl₄liver injury serum ALT, AST and TBiL level （P<0.01）.（3）Gavage polysaccharide twoweeks CCl₄acute liver injury induced the chick serum MDA content with the blankgroup, model group was significantly （P<0.01）. Compared with model group, low,middle and high dose polysaccharide group and positive group can be verysignificantly reduced CCl₄liver injury MDA content （P<0.01）, and with the effect ofincreasing doses of polysaccharide; the GSH activity with the blank group, modelgroup were significantly lower, the difference was significant （P<0.01）. Comparedwith model group, the the various polysaccharide group has different degrees. （4）Observation Group E results, compared with the control group, model group,positive group, Qiling bulk polysaccharides low activity of serum Nagase in the highdose group showed an upward trend （P<0.05or0.01）, CCl₄caninduced the chick liverinjury caused elevated activity of serum Nagase. Positive group, Qiling Sanpolysaccharide low, medium, and high dose group, serum Nagase activity weresignificantly lower than the model group （P<0.01）, the Qiling scattered thepolysaccharides and bifendate can to varying degrees to that inhibition of CCl₄leadabnormally elevated serum Nagase activity.（5）Gavage the CCl₄trials chicken, livertissue showed obvious steatosis, blisters degeneration and necrosis of liver cells, thetest found that the low the Qiling bulk crude polysaccharide, medium and high dosegroups the degree of liver injury than the model group, by gavage four weeks after thevisible vacuolar degeneration and fatty degeneration of the liver tissue wassignificantly reduced or even disappear, only a small amount of necrosis.F group:（1）After we fed chicken polysaccharide four weeks, compared with thecontrol group, the liver index only model group was significantly difference （P<0.05）.Compared with model group, each group was significantly or very significantlyreduced, low-dose group, middle-dose group, and high doses of polysaccharide groupcompared with model group liver index difference decreased significantly （P<0.01）.Compared with the positive group, low-dose group, middle-dose group, and high dosepolysaccharide group liver index difference was not significant （P>0.05）, but theresults are better than the positive group.Gavage polysaccharide four weeks, CCl₄induced chicks acute liver injury serum ALT AST activity and TBiL of changes in thecontent and blank group, the polysaccharide group and positive group of liver injuryhave eased, as the dose increases, the effect is more obvious. Model group, liverinjury and E group has been reduced, may be related to the liver self-recoverycapabilities.（3）Group F CCl₄acute liver injury caused by the change of chicks serumMDA content compared with the control group, model group increased significantly（P<0.05）. Compared with model group, the various polysaccharide group and thepositive group are basically back to normal levels; and GSH activity with the controlgroup was significant difference （P<0.05）. Compared with model group, each polysaccharide group has increased to varying degrees, the high-dose groupdifferences extremely significant （P<0.01）.（4）Group F results showed that comparedwith the control group, in addition to the model group, the other groups were recoverytrend differences with the control group was not significant （P>0.05）, Description theQiling scattered polysaccharide CCl₄-induced liver injury protection and promotion ofrepair. The Qiling scattered crude polysaccharide low, medium and high dose groupand positive group serum NAGase activity were significantly lower than those in themodel group （P<0.01）.（5）F liver repair capacity than the model group, Qiling Sancrude polysaccharides have the ability to promote repair liver damage.