Punicic acid (Trichosanic acid) is a naturally occurring conjugated linolenic acid and polyunsaturated fatty acid that is anti-obesity and anti-diabetic through activation of PPARα, PPARβ, PPARγ, and inhibition of NF-κB; anti-inflammatory through inhibition of cyclooxygenase (COX) and lipoxygenase (LOX); improves neuroinflammation; and prevention of osteoporosis.

Punicic acid at 10 μM for 4 min strongly inhibits TNF-α-induced excessive ROS production in neutrophils, without affecting ROS production triggered by fMLP or Phorbol 12-myristate 13-acetate [1].
Punicic acid at concentrations ranging from 0 to 40 μM for 30 min reduces TNF-α-induced p47phox phosphorylation starting at 10 μM [1].
Punicic acid at 10 μM for 30 min inhibits NADPH oxidase activation in neutrophils [1].
Punicic acid at 0 to 40 μM for 48 h shows a concentration-dependent anti-proliferative effect on MDA-ERα7 and MDA-wt cells [2].
Punicic acid at 40 μM for 48 h induces apoptosis in MDA-ERα7 and MDA-wt cells and increases the percentage of cells in the G2/M phase. This apoptotic effect is completely blocked by the presence of 20 μM α-tocotrienol[2].
The anti-proliferative effect of Punicic acid at 5 to 80 μM for 48 h is partially inhibited by 4 μM BIM in MDA-ERα7 and MDA-wt cells [2].

Oral administration of Punicic acid (400 μg, once daily for ten days) significantly alleviated colonic damage induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS) in male Wistar rats, resulting in only mild inflammatory infiltration and scattered mucosal erosions [2].