5-Heptadecylresorcinol

5-Heptadecylresorcinol (AR-C17), a phenolic lipid component, is also an orally active mitochondrial protector. 5-Heptadecylresorcinol improves mitochondrial function via sirtuin3 signaling pathway, thus alleviates endothelial cell damage and apoptosis. 5-Heptadecylresorcinol induces sirtuin3-mediated autophagy. 5-Heptadecylresorcinol reduces the atherosclerotic plaques in the aortic root region of mice heart. 5-Heptadecylresorcinol can be used for research of atherosclerosis prevention and obesity^[1][2]. In Vitro:5-Heptadecylresorcinol (0, 0.5, 1, and 2 µM; 24 h) alleviates mitochondrial dysfunction through upregulation of SIRT3 in HUVECs^[1].
5-Heptadecylresorcinol alleviates inflammatory conditioned medium (CM) induced adipocyte lipolysis and mitochondrial damage, accompanied by attenuated mitochondrial reactive oxygen species production and mitochondrial membrane depolarization^[2].
5-Heptadecylresorcinol (5, 10 and 15 μM; 24 h) significantly prevents CM-induced adipocyte lipolysis by decreasing the release of glycerol in 3T3-L1 adipocytes^[2].
5-Heptadecylresorcinol (5, 10 and 15 μM; 24 h) ameliorates mitochondrial dysfunction in adipocytes induced by CM^[2].
In Vivo:5-Heptadecylresorcinol (30 mg/kg, 150 mg/kg; po daily for 16 weeks) improves the lipid metabolism in HFD-fed ApoE^−/− mice^[1].
5-Heptadecylresorcinol (30 mg/kg, 150 mg/kg; po daily for 16 weeks) increases the body weight of mouse, and alleviates adipose tissue macrophage infiltration and mitochondrial dysfunction^[2].