Linoleate (sodium)

Linoleate sodium is an orally active IL8 regulator via the JNK and NF-κB pathway. Linoleate sodium can change the composition of fatty acids and the production of metabolites in cells. Linoleate sodium has anti-inflammatory, immune-regulating, and tumor cell growth-affecting activities^{[1][2][3][4][5][6][7][8][9]}. In Vitro: Linoleate (0.125-1.0 mM, 24 h (for viability test)) sodium increases viability of hepatocytes and regulates TG accumulation in goose primary hepatocytes^[1].
Linoleate (100-1000 μM, 9 h) sodium combined with palmitate (500 μM) significantly inhibits IL8 (mRNA and protein) production in Huh7 and HepG2 cells, below that of palmitate alone^[2].
In Vivo: Linoleate (in the form of high-linoleate safflower oil, 10% (w/w), p.o., dietary, 4 weeks) sodium preserves cardiolipin and attenuates mitochondrial dysfunction in the failing rat heart^[3].
Linoleate (in the form of a diet containing 15% (w/w) safflower oil; p.o., through diet) sodium reduces the induction of fatty acid synthetase activity in rat liver^[4].
Linoleate (in the form of linoleate-enriched safflower oil, 100 ppm, dietary) sodium increases arachidonic acid (20:4_n-6) levels in the serum of mice with antigen-induced antibodies and allergic reactions^[5].
Linoleate (in the form of linoleate-enriched safflower oil, corresponding to an 18:2_n-6/18:3_n-3 ratio of 127; dietary) sodium attenuates gastric mucosal damage induced by ethanol, ischemia/reperfusion, and water immersion stress in a rat experimental gastric ulcer model^[6].
Linoleate sodium (1 mg/mouse; ip; 1 time) significantly increases the median survival of mice inoculated with EAT cells from 18 days to 48 days, and completely inhibited tumor growth in more than 40% of mice^[7].
Linoleate (in the form of linoleate-rich safflower oil, 10% of the semi-purified diet; fed) sodium makes ICR mice more sensitive to pentobarbital, as manifested by a shorter onset of anesthetic effect and a longer duration of anesthetic^[8].
Linoleate (in the form of linoleate-rich safflower oil corresponding to an 18:2_n-6/18:3_n-3 ratio of less than 0.1; fed) can reduce urine protein levels, plasma urea nitrogen levels, glomerular crescent formation, and fibrinoid necrosis in rats with crescent-type anti-glomerular basement membrane nephritis, while increasing the proportion of arachidonic acid (20:4_n-6) in glomerular phospholipids^[9].