87205-99-0
87205-99-0 结构式
基本信息
丹参酮 二水合物
二氢丹参酮Ⅰ对照品,
二氢丹参酮I(标准品)
二氢丹参酮 Ⅰ, 来源于丹参
二氢丹参酮 I, 来源于丹参
DIHYDROTANSHINONE I 二氢丹参酮I
DIHYDROTANSHINONE I 二氢丹参酮I 标准品
product/153057
Dihydrotanshinone I
Cannabisin A standard
15,16-Dihydrotanshine I
Dihydrotanshinone I 87205-99-0
Dihydrotanshinone Ⅰ, froM Salvia Miltiorrhiza
Dihydrotanshinone I, 15,16-Dihydrotanshinone I
Dihydrotanshinone I, 98%, from Salvia miltiorrhiza
1,6-DiMethyl-1,2-dihydrophenanthro[1,2-b]furan-10,11-dione
物理化学性质
安全数据
常见问题列表
In lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs), DHT (10 nM) decreases lectin-like ox-LDL receptor-1 (LOX-1) and NADPH oxidase 4 (NOX4) expression, reactive oxygen species (ROS) production, NF-κB nuclear translocation, ox-LDL endocytosis and monocytes adhesion. Dihydrotanshinone I induces caspase dependent apoptosis induced in HCT116 cells. Dihydrotanshinone I induces concentration and ROS dependent caspase activation. Apoptosis induced by Dihydrotanshinone I is completely prevented by Z-VAD-fmk. Apoptosis induced by Dihydrotanshinone I is significantly inhibited by pretreatment of Z-LEHD-fmk but only is partially inhibited by Z-IETD-fmk. Apoptosis induced by Dihydrotanshinone I is significantly increased by caspase-2 knockdown.
DHT (10 and 25 mg/kg) significantly attenuates atherosclerotic plaque formation, alteres serum lipid profile, decreases oxidative stress and shrinks necrotic core areas in ApoE -/- mice. DHT dramatically inhibits the enhanced expression of LOX-1, NOX4, and NF-κB in aorta. Dihydrotanshinone I (1, 2, 4 mg/kg) treatment can improve cardiac function, reduce infarct size, ameliorate the variations in myocardial zymogram and histopathological disorders, decrease 20-HETE generation, and regulate apoptosis-related protein in myocardial ischemia-reperfusion rats.