PLoS One. 2016 ;11(12):e0168219. Epub 2016 Dec 14. PMID: 27973574
Ginkgolide B Exerts Cardioprotective Properties towards Doxorubicin-Induced Cardiotoxicity by Regulating Reactive Oxygen Species, Akt and Calcium Signaling Pathways In Vitro and In Vivo.
The purpose of this research was to guage the impact of Ginkgolide B (GB) on doxorubicin (DOX) induced cardiotoxicity in vitro and in vivo. Rat cardiomyocyte cell line H9c2 was pretreated with GB and subsequently subjected to doxorubicin therapy. Cell viability and cell apoptosis have been assessed by MTT assay and Hoechst staining, respectively. Reactive oxygen species (ROS), Akt phosphorylation and intracellular calcium have been equally decided with a view to discover the underlying molecular mechanism. To confirm the in vivo therapeutic impact of GB, we established a mouse mannequin of cardiotoxicity and decided left ventricle ejection fraction (LVEF) and left ventricular mass (LVM). The in vitro experimental outcomes indicated that pretreatment with GB considerably decreases the viability and apoptosis of H9c2 cells by lowering ROS and intracellular calcium ranges and activating Akt phosphorylation. Within the in vivo research, we recorded an improved LVEF and a decreased LVM within the group of cardiotoxic rats handled with GB. Altogether, our findings anticipate that GB exerts a cardioprotective impact via attainable regulation of the ROS, Akt and calcium pathways. The findings recommend that mixture of GB with DOX in chemotherapy might assist keep away from the cardiotoxic unwanted side effects of GB.