| The purpose of this experiment is to provide a reference for the in-depth study of duck ascites syndrome by studying the morphological changes caused by duck ascites syndrome and exploring its mechanism.The Shan Ma ducks with hepatitis B virus(DHBV)detected by viral group sequencing and suffering from ascites were set as the pathological group(Dis),and the Shan Ma ducks of the same age without lesions and DHBV infection were set as the control group(Nor),30 Shan Ma ducks in each group.The clinical symptoms of the Shan Ma ducks were recorded,and the morphological changes of the Shan Ma duck ascites syndrome were observed by anatomical examination,HE staining,Masson staining and transmission electron microscopy,and then combined with biochemical index tests and apoptosis assays to assess their liver function.Finally,transcriptome sequencing and untargeted metabolomics sequencing techniques were used to analyze the dynamic changes of transcript levels and metabolic levels in the liver tissue of Shan Ma ducks,respectively.The test results are as follows:(1)Compared with the control group,the abdomen of Shan Ma ducks in the pathology group was bulging and had a water balloon-like fluctuating feeling when touched.A large amount of yellow fluid was visible on dissection,and its liver was enlarged,yellowish and white in color,hard and brittle in texture.The liver plate became narrow and interrupted,the confluent area was infiltrated with inflammatory cells,the small bile ducts were moderately and severely squeezed and atrophied,and a large amount of pink-stained material was deposited in the liver sinusoids,which was identified as collagen fiber hyperplasia.The hepatocytes were structurally deformed,with broken cell membranes,cleaved nuclei,most organelles damaged,swollen endoplasmic reticulum,reduced ribosomes,and broken mitochondrial ridges.(2)Compared with the control group,the serum biochemical indexes of ALB content significantly decreased(P < 0.05),GLO content significantly increased(P < 0.05),AST,ALT and ALP extremely significantly increased(P < 0.01)in the pathological group of Shan Ma ducks,whose liver underwent apoptosis,suggesting liver dysfunction in the pathological group.The pathogenic test results showed DHBV infection in the liver of the mountain mock Shan Ma duck in the pathology group.(3)At the transcription level,676 differentially expressed genes were detected in the liver tissues of Shan Ma ducks with ascites syndrome compared to controls,and these differentially expressed genes were significantly enriched in protein processing modification pathways,ECM receptor interactions,fructose and mannose metabolism,autophagy,protein transport and ABC transporter pathways in the endoplasmic reticulum.(4)At the metabolic level,47 metabolic differentials were screened in liver tissues of sage-grouse Shan Ma ducks suffering from ascites syndrome compared to controls,affected by biochemical metabolic pathways such as synthesis and degradation of ketone bodies,valine,leucine and isoleucine biosynthesis/degradation and propionate metabolism,and the metabolites of interest in these pathways were acetoacetic acid and 2-oxobutyric acid.In summary,this study found that liver fibrosis may be the key to the formation of Shan Ma duck ascites syndrome,which may be caused by DHBV infection.The omics results provide ideas and directions for the study of molecular mechanism of Shan Ma duck ascites syndrome. |