1-HEXACOSANOL 激活 AMPK 和肝脏自噬并抑制 SREBP2，导致降胆固醇活性和肝脏脂肪变性的改善。

Hexacosanol activates AMPK and hepatic autophagy and inhibits SREBP2, resulting in hypocholesterolemic activities and improvement of hepatic steatosis.

Plasma, hepatic cholesterol concentrations and hepatic steatosis were significantly reduced in high-fat-fed mice orally administered with hexacosanol (0.7 mg/kg body weight/day) for 8 weeks compared to those of vehicle-fed control mice (-15 and -40%, respectively)[1]. Diabetes was induced in 8-week-old male Sprague-Dawley rats by administering an intraperitoneal injection of streptozotocin (50 mg/kg). The rats were divided into four groups and maintained for 8 weeks: control rats, diabetic rats without treatment with N-hexacosanol, and diabetic rats treated with N-hexacosanol (2 mg/kg and 8 mg/kg i.p. every day). Although N-hexacosanol failed to modify the diabetic status, increases in serum creatinine as well as in kidney weight were significantly reduced. The malonaldehyde and transforming growth factor beta-1 (TGF-beta1) concentrations as well as the protein kinase C (PKC) activities in the diabetic kidney were significantly higher than those of the control, which were decreased by treatment with N-hexacosanol. Histological examinations revealed that N-hexacosanol significantly ameliorated diabetic-induced tubulointerstitial pathological changes[2].

506-52-5

C26H54O

382.717

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years