| Duck viral hepatitis (DVH) is an acute and highly contagious disease of young ducklings caused by duck hepatitis virus A1type (DHAV-1), characterized with high mortality and liver lesions included haemorrhage, fat degeneration and necrosis. Even though nearly two years whole DHAV1genome sequences got the attention of people, the domestic many researchers’attention focused on the study of etiology, and studies on the pathogenesis of DVH is still limited in the histology and serological levels. DHAV-1is the most widely distributed and can cause mortality higher than90%in ducklings in1week of age. Natural infection case was associated with age,1～2weeks is the peak of the disease.35day-old ducks had no clinical signs when they were infected with DHAV-1. why? For duck liver lipid metabolism many researchers focused in8～12week-old ducks under over feeding among different breed ducks. However, there is little information regarding lipid metabolism in any breed ducklings, and no such information is available for Cherry valley broiler ducks. To understand the possible relationship between the susceptibility to DHAV and the liver lipid content in ducklings, the age-related differences make lipid metabolisms of ducklings worthy of investigation. In this first study we examined the liver lipid metabolism by serology and liver histology under ad libitum feeding in growing broiler ducks.Moreover, The plenty of lipid may induce lipid peroxidation and free redical. Once the ducks were evoked by stress such as virus, they were apt to liver injury. So in the second part, we will focus the liver lipid peroxidation, lipid metabolism related genes and the changes of inflammatory factors in the DHAV-1animal models, so as to clarify damage mechanism of the duck hepatitis virus to duckling liver.1. The characteristics of liver lipid metabolism in the cherry valley meat duck with3-35daysTo understand the possible relationship between the susceptibility to DHAV and the liver lipid content in ducklings, the age-related differences make lipid metabolisms of ducklings worthy of investigation. The change of serology and duck liver histology, dynamic liver fat metabolism regulation were carried out within35days of age duck.Results showed that the content of crude fat in liver tissue were greater than10%, of which3d was the highest content of crude fat in the liver, can reach38.65%. The most neutral fat of the4d liver was found in liver tissue frozen section with oil red O stainingthe plasma lipid metabolism indicators suggested total bilirubin (TBIL), total cholesterol (TC), high density lipoprotein cholesterol (HDLC) and low density lipoprotein cholesterol (LDLC) decreased from3to7days, and total glycerate (TG) increased, the time of the obvious changes was focused on7,14days of age. The microsomai triglyceride transfer protein (MTP), peroxisome proliferative activated receptor (PPAR) and fatty acid binding protein (FABP) expression in the liver were observed by immunohistochemical method:at the age of14d, the plasma TG rose to the highest, at the same time the expression of MTP decreased. Similarly, at the age of21d, the crude fat content in liver tissue was the lowest and the expression of MTP rose to the highest, which suggested that MTP were involved in TG transshipment in liver cell. PPAR expressed gradually rose and the content of crude fat rapidly declined in the liver tissue at3to28days of age, which suggested the two indexes showed a negative correlation.FABP expression may be closely related to TG synthesis in the liver. Conclusion:1-3weeks is the key period in which intrahepatic lipid were send to other parts of the body.2. The mechanism of duck hepatitis virus on liver damage in the4day-old cherry valley duckPoultry liver contains most macrophages (kupffer cells), under stress, the role of the activated cells in the duck hepatitis virus infection is not clear. In view of the characteristics of duck liver, this research focused on lipid metabolism, free radical and cytokine changes to clarify the possible mechanism of liver injury. At5day post-infection (PID), the live total antioxidant capacity decreased, malonldehyde(MDA) rose2-3PID, nitric oxide (NO) and induciable nitric oxide synthase (iNOS) in2-3d increased, which caused the liver hemorrhage, degeneration necrosis and bile duct epithelial hyperplasia. Fluorescence quantitative PCR detection of cytokines transcription:INFa transcription rose at1PID and then fell, and cytokine IL-1β, IL-10, TNF-a transcription level decreased, serum IL-1β at1PID increased obviously, and serum IL-6had no significant change. Liver cell damage caused blood transaminase increasing quickly, liver MTP expression at1PID decreasing sharply, elevated serum TG, TC, DLDC, abnormal lipid transport inducing liver steatosis. DHAV-1JX caused4day-old duck acute liver damage and sharp liver dysfunction, IBIL rising in the blood, blood ammonia insufficient removal, blood sugar levels dropping, and hepatic coma. Conclusion:DHAV-1JX induced the cytokines weak production in duck liver, but can stimulate duck liver producing large amounts of NO and lipid free radicals. |
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