The chemically induced non-alcoholic fatty liver disease (NAFLD) model is established by administration of chemicals or drugs that cause hepatotoxicity through varying mechanisms.
The combination of low-dose streptozotocin (STZ) with a high-fat diet has been used to model NAFLD in mice, resulting in steatosis, inflammation, fibrosis, and even hepatocellular carcinoma. Carbon tetrachloride (CCl4) can cause liver damage and be administered alone or with a high-fat diet to induce fatty liver or liver fibrosis. The main mechanism is that CCI4 induces an oxidative stress reaction in the liver, resulting in the continuous production and accumulation of harmful lipid and protein peroxidation products, along with a severe necrosis reaction - resulting in the destruction of liver cells’ structure and function. This method has a relatively short induction period - however, the pathogenesis and histological morphology are quite different from those of human fatty liver, and these drugs may be highly toxic and may cause animal death.
Detection Items: Body weight, food intake, serum biochemical test (alanine aminotransferase, aspartate aminotransferase, serum total cholesterol, triglyceride content, etc.), pathological analysis of liver tissue (liver tissue H & E staining, oil red).