动物造模,非酒精性脂肪性肝病 z-bio 2023-06-05 1161

　　Objective To investigate the effect of Helicobacter hepatica infection on high-fat diet-induced non-alcoholic fatty liver disease.

　　Methods Twenty 6-week-old male BALB/c mice were randomly divided into 4 groups with 5 mice in each group, namely blank control group, HFD group, H.h group and H.h+HFD group. The H.h+HFD group was fed with high-fat diet after infection with H.h. The mice in each group were sacrificed after being fed for 12 weeks, and the serum levels of triglyceride (TG), alanine transaminase (ALT) and aspartate aminotransferase (AST) in the serum of mice in each group were detected. The liver lesions were evaluated by oil red O staining, Sirius red staining, hematoxylin-eosin staining, real-time quantitative PCR and immunohistochemistry.

　　Results The serum levels of TG, ALT and AST in the H.h+HFD group were significantly higher than those in the blank control group (all P<0.05), and higher than those in the H, h group and HFD group (all P<0.05). The liver tissue of H, h+HFD mice showed fat deposition, hepatocyte ballooning degeneration and punctate necrosis, and massive deposition of collagen fibers; Hh group showed inflammatory cell aggregation and a small amount of collagen fiber deposition; HFD group showed lipid droplet accumulation and accumulation of collagen fibers. Steatosis, and a small amount of collagen fiber deposition. H, Interleukin-6 (IL-6), IL-1β, transforming growth factor-β (TGF-β) and tumor necrosis factor-α in the liver of mice in the h+HFD group (tumor necrosis factor-α, TNF-α) mRNA transcription levels were significantly higher than those of the other three groups (all P≤0.05), and α-SMA and Collagen I proteins were also significantly expressed.

　　Conclusion H, h infection can promote the development of high-fat diet-induced non-alcoholic fatty liver disease in mice.