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In Vitro: Ginsenoside Rb3 suppresses OGD-Rep-induced cell apoptosis by the suppression of ROS generation. Ginsenoside Rb3 inhibits the upregulation of phospho-IκB-α and nuclear translocation of NF-κB subunit p65 which are induced by ORD-Rep injury. In addition, the extract also inhibits the OGD-Rep-induced increase in the expression of inflammation-related factors, such as IL-6, TNF-α, monocyte chemotactic protein-1 (MCP-1), MMP-2 and MMP-9 [1]. Ginsenoside Rb3 decreased cell cycle progression from G(0)/G(1) to S phase. Furthermore, ginsenoside Rb3 significantly attenuated the expression of mRNA of proto-oncogene c-myc, c-fos and c-jun [2]. Ginsenoside Rb3 (0.1-10 micromol/L) significantly increased cell viability and inhibited LDH release in a dose-dependent manner on the ischemic model. In addition, ginsenoside Rb3 also significantly inhibited ischemic injury-induced apoptosis, [Ca(2+)](i) elevation, and decrease of MMP [3].
In Vivo: Ex vivo treatment with Rb3 concentration-dependently augmented endothelium -dependent relaxations, suppressed endothelium-dependent contractions and reduced ROS production and expressions of NOX-2, NOX-4 and p67(phox) in arterial rings from SHR. Rb3 treatment also normalized angiotensin II (Ang II)-stimulated elevation in ROS and expression of NOX-2 and NOX-4 in arterial rings from WKY rats [4].

 | | Dave Gao Sales Manager, Star Ocean Ginseng Professional Services Tel: +86 512 81662860 Mobile: +86 13776237441 Fax: +86 512 52856900 Email: sales@star-ocean-biotech.com, star-ocean@vip.163.com Address: High Tech Industrial Development Zone-Tongji Science and Technology Plaza, Changshu, Suzhou, China. |