• Modeling Mechanism：

  Sodium taurocholate can activate the Hippo-YAP/TAZ signaling pathway, downregulate the expression of MST1 and LATS1/2, and upregulate SAV1, MOB1 and downstream Cyclin D1, CYR61, and CTGF genes. At the same time, it regulates bile acid metabolism, activates the FXR-SHP signaling axis, maintains bile acid homeostasis, and synergistically promotes hepatocyte proliferation and liver regeneration, accompanied by mild liver damage.

• Related Products：

  Sodium taurocholate (TWA2417)

• Modeling Method：

  Experimental Subject：

  Rats, Wistar, Male, 230–270 g

  Dosage and Administration Route：

  0.5% Sodium taurocholate, Administered orally via feed

  Dosing Frequency and Duration Model：

  Postoperative continuous administration

• Validation：

  The regeneration rate of unligated liver lobes was significantly increased, and the proportion of Ki67 positive hepatocytes increased; serum and liver tissue TBA levels were elevated, FXR and SHP gene expression was upregulated, and Cyp7a1 expression was downregulated; the expression of key genes in the Hippo signaling pathway was altered; and serum ALT, AST, and TBil levels were slightly elevated.

*Precautions： All rats were sacrificed in batches on days 1, 2, 3, 5, and 7 after surgery; fasting was required for 12 hours before modeling; the concentration of sodium taurocholate in the feed was strictly controlled at 0.5% to avoid excessive concentration leading to severe liver damage.

*References：Ge X,et,al. Sodium taurocholate promotes liver regeneration after portal vein ligation in rats. Sci Rep. 2025 Nov 26;15(1):45436.

• Modeling Mechanism：

  After sodium taurocholate is retrogradely injected into the bile and pancreatic ducts, it activates the release of pancreatic digestive enzymes (such as lipase), triggering pancreatic autodigestion; at the same time, it induces oxidative stress (glutathione depletion, enhanced lipid peroxidation), inhibits the activity of serine/threonine protein phosphatases (PP1, PP2A), and upregulates pro-inflammatory cytokines; in obese states, increased abdominal fat is prone to necrosis, releasing large amounts of free fatty acids, which exacerbates pancreatic and systemic inflammatory responses.

• Related Products：

  Sodium taurocholate (TWA2417)

• Modeling Method：

  Experimental Subject：

  Rats, Zucker, Male, Lean rats 308±25g, obese rats 433±34g

  Dosage and Administration Route：

  3.5% sodium taurocholate, 0.3ml dissolved in physiological saline, retrograde injection into the bile duct via the duodenum

  Dosing Frequency and Duration Model：

  Single dose

• Validation：

  The pancreatic glutathione (GSH) level decreased, the oxidized glutathione (GSSG) level increased, and the activities of PP1 and PP2A decreased; the plasma and ascites fluid levels of isoprostaglandins and malondialdehyde (MDA) increased, and the plasma and ascites fluid levels of triglycerides and free fatty acids increased significantly.

*Precautions： All rats were sacrificed in batches at 0, 1, and 6 hours after modeling, and pancreatic, adipose tissue, plasma, and ascites samples were collected simultaneously.

*References：Pereda J,et,al. Obese rats exhibit high levels of fat necrosis and isoprostanes in taurocholate-induced acute pancreatitis. PLoS One. 2012;7(9):e44383.