Background:

IC50: N/A

Schisandrin B (Sch B), the most abundant dibenzocyclooctadiene lignin, is isolated from the fruit of Schisandra chinensis.

In vitro: Schisandrin B has early been found to inhibit in vitro lipid peroxidation by NADPH/ ascorbate and cysteine/ferric systems in isolated rat liver microsomes. In addition, using electron spin resonance measurement, Sch B was shown to scavenge both in vitro hydroxyl and superoxide radicals. In contrast to that α-tocopherol produced prooxidant and antioxidant effect on Fe3+-induced lipid peroxidation, Sch B could only inhibit the peroxidation reaction [1].

In vivo: Five days after a single injection of doxorubicin (Dox) administration (20 mg/kg IP), left ventricular (LV) performance in mice was depressed significantly and was improved by Sch B treatment. Sch B could prevent the Dox-induced lipid peroxidation increase, nitrotyrosine formation, as well as metalloproteinase activation in the heart. Additionally, the increased expression of phosphop38 MAPK and phospho-MAPK activated mitogen kinase 2 levels by Dox were found to be suppressed by Sch B treatment significantly. Moreover, Sch B also attenuated Dox-induced higher expression of LV proinflammatory cytokines, myocardial apoptosis, cardiomyocyte DNA damage, caspase-3 positive cells and phopho-p53 levels in mice [2].

Clinical trial: N/A

参考文献:
[1] Mak DH,Ip SP,Li PC,Poon MK,Ko KM.  Effects of Schisandrin B and alpha-tocopherol on lipid peroxidation, in vitro and in vivo. Mol Cell Biochem.1996 Dec 20;165(2):161-5.
[2] Thandavarayan RA,Giridharan VV,Arumugam S,Suzuki K,Ko KM,Krishnamurthy P,Watanabe K,Konishi T.  Schisandrin B prevents doxorubicin induced cardiac dysfunction by modulation of DNA damage, oxidative stress and inflammation through inhibition of MAPK/p53 signaling. PLoS One.2015 Mar 5;10(3):e0119214.