Dihydrotanshinone I is a natural compound extracted from Salvia miltiorrhiza Bunge which has been widely used for treating cardiovascular diseases. Dihydrotanshinone I exhibits entry-blocking effect for MERS-CoV.

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.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

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.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

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.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

• . Zhao W, et al. Dihydrotanshinone I Attenuates Atherosclerosis in ApoE-Deficient Mice: Role of NOX4/NF-κB Mediated Lectin-Like Oxidized LDL Receptor-1 (LOX-1) of the Endothelium. Front Pharmacol. 2016 Nov 8;7:418. eCollection 2016.  [Content Brief]

  . Wei Y, et al. The cardioprotection of dihydrotanshinone I against myocardial ischemia-reperfusion injury via inhibition of arachidonic acid ω-hydroxylase. Can J Physiol Pharmacol. 2016 Dec;94(12):1267-1275. Epub 2016 Jun 24.  [Content Brief]

  . Wang L, et al. Dihydrotanshinone I induced apoptosis and autophagy through caspase dependent pathway in colon cancer. Phytomedicine. 2015 Nov 15;22(12):1079-87  [Content Brief]

  [4]. Ji Yeun Kim, et al. Safe, High-Throughput Screening of Natural Compounds of MERS-CoV Entry Inhibitors Using a Pseudovirus Expressing MERS-CoV Spike Protein. Int J Antimicrob Agents. 2018 Nov;52(5):730-732.  [Content Brief]