Description |
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].
|
Target |
SIRT3
|
In Vitro |
5-Heptadecylresorcinol(0、0.5、1 和 2 µM;24 小时)通过上调 HUVEC 中的 SIRT3 减轻线粒体功能障碍[1]。 5-Heptadecylresorcinol 减轻了炎症条件培养基 (CM) 诱导的脂肪细胞脂肪分解和线粒体损伤,同时减弱了线粒体活性氧的产生和线粒体膜去极化[2]。 5-Heptadecylresorcinol(5、10 和 15 μM;24 小时)通过减少 3T3-L1 脂肪细胞中甘油的释放显着防止 CM 诱导的脂肪细胞脂肪分解[2]。 5-Heptadecylresorcinol(5、10 和 15 μM;24 小时)改善 CM 诱导的脂肪细胞线粒体功能障碍[2]。 Western Blot Analysis[2] Cell Line: 3T3-L1 adipocytes Concentration: 5, 10 and 15 μM Incubation Time: 24 hours Result: Increased the expression of UCP1, COX IV, PGC-1α, DRP1 and MFN2 proteins.
|
In Vivo |
5-Heptadecylresorcinol(30 mg/kg、150 mg/kg;每日口服,持续 16 周)改善高脂饮食喂养的 ApoE−/− 小鼠的脂质代谢[1]。 5-Heptadecylresorcinol(30 mg/kg、150 mg/kg;每天口服,持续 16 周)增加小鼠体重,减轻脂肪组织巨噬细胞浸润和线粒体功能障碍[2]。 Animal Model: C57BL/6J mice[1][2] Dosage: 30 mg/kg, 150 mg/kg Administration: PO; daily for 16 weeks Result: Lowered serum total cholesterol, triglyceride, VLDL-C, and LDL-C levels[1]. Reduced adipose tissue macrophage infiltration from high-fat diet induced obese C57BL/6J mice[2].
|
Density | 1.0±0.1 g/cm3 |
Boiling Point | 478.0±15.0 °C at 760 mmHg |
Flash Point | 202.6±15.0 °C |
Exact Mass | 348.302826 |
PSA | 40.46000 |
LogP | 9.72 |
Vapour Pressure | 0.0±1.2 mmHg at 25°C |
Storage condition | 2-8°C |