• Modeling Mechanism：

  After retrograde injection of taurocholic acid sodium salt hydrate 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：

  Taurocholic acid sodium salt hydrate (T1138)

• Modeling Method：

  Experimental Subject：

  Rats, Zucker, Male, Lean rats 308±25g, obese rats 433±35g

  Dosage and Administration Route：

  3.5% sodium taurocholate, 0.3 ml 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.

• Modeling Mechanism：

  Taurocholic acid sodium salt hydrate 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：

  Taurocholic acid sodium salt hydrate (T1138)

• Modeling Method：

  Experimental Subject：

  Rat, Wistar, Male, 230-270g

  Dosage and Administration Route：

  0.5% Taurocholic acid sodium salt, Administered orally mixed with 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.