• Modeling Mechanism：

  Thioacetamide (TAA), a potent hepatotoxic compound, is metabolized and activated in the liver of rats to produce thioacetamide S-oxide and sulfinic acid esters. Its thiosulfate group induces oxidative stress through oxidation, generating reactive oxygen species (ROS). ROS damages hepatocyte mitochondrial function, increases cell membrane permeability and intracellular Ca²⁺ concentration, leading to hepatocyte necrosis. At the same time, it activates Kupffer cells to release pro-inflammatory factors (TNF-α), induces the activation and differentiation of hepatic stellate cells (HSCs) into myofibroblasts, and synthesizes large amounts of extracellular matrix such as collagen, forming liver fibrosis. Long-term modeling can progress to cirrhosis, mimicking the pathological process of chronic liver injury-fibrosis-cirrhosis in humans.

• Related Products：

  Thioacetamide (T35367)

• Modeling Method：

  Experimental Subject：Rats, Male Wistar rats, body weight 150–175 g

  Dosage and Administration Route：① Core modelling: Thioacetamide (200 mg/kg) dissolved in sterile saline solution administered via intraperitoneal injection; ② Control treatment: Control group administered equal volume saline solution via intraperitoneal injection; all other housing and treatment conditions identical; ③ Intervention verification group (optional): Concurrent administration of hepatoprotective agent (e.g., Olivia aromatic plant extract TO-EtOH/TO-EtOAc), 200–400 mg/kg, Oral, Continuous for 4 weeks (administered 1 hour after Thioacetamide injection); ④ Supportive therapy: Subcutaneous injection of 10% glucose and lactated Ringer's solution (1:1)

  Dosing Frequency and Duration Model：Administered three times weekly for four consecutive weeks

• Validation：

  1. Biochemical Indicators: - Liver Function: Serum ALT, AST, and ALP levels were significantly elevated (199%, 313%, and 235%, respectively), and total bilirubin was elevated by 289% (p<0.001), indicating hepatocellular damage; - Oxidative Stress: Liver tissue malondialdehyde (MDA) was elevated by 178%, and reduced glutathione (GSH) was decreased by 66% (p<0.001), reflecting oxidative damage; - Inflammatory Factors: Liver tissue TNF-α levels were elevated by 200% (p<0.001), indicating inflammatory activation; 2. Pathological Indicators: - HE Staining: Hepatocellular degeneration and necrosis, extensive mononuclear cell infiltration in the portal vein area, portal vein-portal vein bridging fibrosis, and destruction of liver lobule structure; - Sirius Red Staining: The proportion of collagen fiber area in liver tissue was significantly increased, and the fibrosis score (0-3 points) was significantly higher than that in the control group; 3. Immunohistochemical Indicators: - α- Smooth muscle actin (α-SMA): Strong positive expression in liver tissue (significantly increased area%), suggesting activation of hepatic stellate cells (p<0.001).

*Precautions：

*References：Ahmed RF,et,al. Phenolic-rich extracts of Teucrium oliverianum confer protection against thioacetamide-induced liver fibrosis in rats: Insights from metabolomics, biochemical and histopathological analysis. PLoS One. 2025 Sep 2;20(9):e0330595.