Study On Oxidative Damage Of Liver Tissue Of SPF Chicken Embryos By FAdV-4 Fushun Strain

Hydropericardium hepatitis syndrome(HHS)is a highly contagious infectious disease caused by serotype 4 avian adenovirus(Fowl adenovirus serotype-4,FAd V-4).The disease first erupted in the Angolan region of Pakistan in 1987,so it is also known as the poultry "Ankara disease." It has occurred in many countries such as Hungary,India,the United States,Brazil,and Poland.FAd V-4 infection can cause immunosuppression of the body,leading to increased infectivity of other diseases.After poultry infection,pericardial effusion and liver necrosis were the main pathological changes,but the impact of FAd V-4 on oxidative damage of avian liver tissue is still unclear.This experiment will investigate the oxidative damage caused by FAd V-4 on SPF chicken embryo liver tissue.In this study,the FAd V-4 Fushun strain preserved in the laboratory was used to inoculate the 11-day-old SPF chicken embryo chorioallantoic cavity.After 7 days of infection,After 7 days of infection,necropsy and observe the damage.At the same time,the chicken embryo liver tissue was taken and a part of liver tissue was fixed with 10% formalin for paraffin sectioning and histopathological observation after HE staining;Another part of liver tissue is used for liver tissue oxidative damage research:First,related indicators of liver tissue oxidative damage: using kit to detect malondialdehyde(MDA)content,total superoxide dismutase(SOD)and glutathione peroxidase(GSH-Px)activity in chicken embryo liver;the second is to investigate the Nrf2/HO-1 pathway of oxidative damage in liver tissue: the m RNA level of Nrf2 and HO-1 was detected by real-time quantitative PCR;the expression of Nrf2 protein in cytoplasm and nucleus of hepatocytes by Western blotting,to explore the mechanism of oxidative damage of FAd V-4 on SPF chicken embryo liver.Results: After embryos infected with FAd V-4,Chicken embryos showed slow development.The liver showed yellow-green color and bleeding spots on the surface.Histopathological results showed that the infected embryonic liver cells suffered from severe blisters denaturation,nucleus fragmentation,dissolution,central venous and sinusoidal dilatation,and a large amount of red blood cells.Compared with the control group,the MDA content of the experimental group was significantly increased(p<0.01),and the SOD activity was significantly decreased(p<0.01),indicating that FAd V-4 can destroy the redox homeostasis of chicken embryo liver.The expression of Nrf2 protein in cytoplasm decreased significantly(p<0.05),and the expression of Nrf2 protein in the nucleus increased significantly(p<0.05).The expression of Nrf2 and HO-1 m RNA in the experimental group decreased significantly(p<0.01).The results indicated that FAd V-4 can activate Nrf2 and undergo nuclear translocation,but inhibit the expression of Nrf2/HO-1 pathway key factors Nrf2 and HO-1 in hepatocytes.In summary,SPF chicken embryos infected with Fushun strain FAd V-4,can cause obvious ocular pathological changes and histopathological damage,and induce oxidative damage in the liver.The expression of key factors in the Nrf2/HO-1 pathway suggests that FAd V-4 may induce oxidative damage in the liver of SPF chicken by down-regulating the Nrf2/HO-1 pathway.The results of this study provide a theoretical basis for revealing the oxidative damage mechanism of FAd V-4 infected SPF chicken liver tissue,and it has laid a foundation for the effective prevention and treatment of pericardial effusion-hepatitis syndrome and the development of key molecular drugs in the Nrf2/HO-1 pathway.