• Modeling Mechanism：

  Arachidonic acid sodium salt, as a precursor to prostaglandin (PG) synthesis, can be converted into inflammatory mediators such as PGE₁ and PGE₂ by prostaglandin synthase infiltrating immune cells such as leukocytes at the site of inflammation. When synergistically with κ-carrageenan or kaolin, it amplifies inflammatory signaling pathways, promotes vasodilation, increased permeability, and interstitial edema, and enhances the foot swelling response. This process can be blocked by nonsteroidal anti-inflammatory drugs (NSAIDs) by inhibiting prostaglandin synthase.

• Related Products：

  Arachidonic acid sodium salt (T84544)

• Modeling Method：

  Experimental Subject：

  Rat, Wistar, Male, 80–100 g

  Dosage and Administration Route：

  100 μg/claw arachidonic acid+1 mg/claw κ-carrageenan, dissolved together in 0.1 mL 0.9% saline, subplantar injection into right hind paw;
  Left hind foot injected with equivalent saline as control

  Dosing Frequency and Duration Model：

  Single dose

• Validation：

  Clinical phenotype: Foot swelling was significantly enhanced after combined administration, reaching a peak at 1.5 hours, and the increase in foot volume was significantly higher than that in the single-drug group (P<0.001). The degree of swelling was a synergistic effect rather than a simple additive effect. Specificity verification: Subcutaneous pretreatment with nonsteroidal anti-inflammatory drugs (indomethacin 5 mg/kg, naproxen 30 mg/kg, phenylbutazone 75 mg/kg) for 0.5 hours significantly inhibited the swelling potentiation effect (inhibition rate 30%-63%); anti-inflammatory steroids (hydrocortisone 100 mg/kg) or acetaminophen (200 mg/kg) had no inhibitory effect.

*Precautions： All rats were sacrificed 1.5 hours after modeling, and foot tissue was collected for the detection of inflammatory mediators.

*References：Lewis AJ,et,al. On the ability of prostaglandin E1, and arachidonic acid to modulate experimentally induced oedema in the rat paw. Br J Pharmacol. 1975 Sep;55(1):51-6.