Arachidonic acid (Immunocytophyt) is a polyunsaturated omega-6 essential fatty acid that serves as a major component of biological membranes and animal phospholipids. It is synthesized from dietary linoleic acid and acts as a precursor to lipid mediators such as prostaglandins, thromboxanes, and leukotrienes. Arachidonic acid can improve cognitive responses and cardiovascular function and is commonly used to induce paw edema models.

Mg2+-ATPase:90 μM, 3H-ouabain:32 μM, NaK-ATPase:75 μM, L-type Ca2+ channel (cardiac myocytes):8.5 μM

METHODS: RAW264.7 and PBMC-derived macrophages were treated with Arachidonic acid (40-80 µM) for 12-24 h and cell viability was determined by CCK8 assay.
RESULTS: Arachidonic acid significantly inhibited macrophage viability in a dose-dependent manner within 12 h, and more inhibition was observed between 12 h and 24 h. Arachidonic acid was also shown to inhibit macrophage viability in a dose-dependent manner. [1]
METHODS: Human breast cancer cells, MDA-MB-231, were treated with Arachidonic acid (8 µM) for 48 h. Caspase activity was measured using a spectrofluorophotometer.
RESULTS: MDA-MB-231 cells stimulated with Arachidonic acid for 48 h showed a significant increase in caspase-3 activity, and Arachidonic acid also induced significant activation of caspase-8 and caspase-9. [2]

METHODS: To test the effect on the inflammatory response, Arachidonic acid (150 mg/kg in 1% CMC Na) was administered orally to C57BL/6 mice with high-fat diet (HFD)-induced cardiac injury every two days for eight weeks.
RESULTS: Arachidonic acid treatment prevented MD2/TLR4 dimerization, induction of inflammatory factors, and tissue damage through TLR4-mediated inflammatory responses in a high-fat diet obese mouse model. [3]