• Modeling Mechanism：

  Zymosan A induces acute inflammation by activating the TLR2 and dectin-1 receptor pathways. On the one hand, it leads to HDL remodeling (enrichment of serum amyloid A, SAA), reduces plasma cholesterol receptor activity and the ability of ABCA1-specific cholesterol efflux; on the other hand, it directly inhibits the cholesterol efflux function of macrophages (in a dose-dependent manner), while downregulating the expression of cholesterol transporters such as ABCG8 in the liver, ultimately hindering the RCT pathway (cholesterol transport from macrophages to plasma to liver to feces), increasing the risk of atherosclerosis.

• Related Products：

  Zymosan A (T78101)

• Modeling Method：

  Experimental Subject：

  Mice, C57BL/6, Male

  Dosage and Administration Route：

  70 mg/kg Zymosan (dissolved in sterile PBS, final concentration 5 mg/mL), 400 μL per animal, intraperitoneal injection (i.p.)

  Dosing Frequency and Duration Model：

  Single dose

• Validation：

  Functional indicators: All steps of the RCT pathway were significantly impaired, with plasma RCT decreasing by 17%, liver RCT decreasing by 22%, and fecal RCT decreasing by 20% (P<0.05); Molecular indicators: Plasma HDL cholesterol decreased by 19% (P<0.01), and SAA levels increased 13-fold (P<0.001); Macrophage ABCA1-dependent cholesterol efflux decreased by 35% (P<0.01); Hepatic ABCG8 mRNA expression was downregulated by 32% (P<0.05);

*Precautions： All mice were sacrificed at predetermined time points after modeling, and plasma, liver, feces, and macrophages were collected for testing.

*References：Malik P,et,al. Zymosan-mediated inflammation impairs in vivo reverse cholesterol transport. J Lipid Res. 2011 May;52(5):951-7.