Background: Rhein, an anthraquinone compound isolated from rhubarb, has been shown to protect the pancreatic β cells from hyperglycemia induced apoptosis in our previous studies.
Purpose: In the present study, we examined whether rhein can protect myocardial cells against ischemia reperfusion (I/R)-induced apoptosis and investigated the underlying mechanism.
Methods: We used an in vitro model of myocardial hypoxia/reoxygenation (H/R) injury. H9c2 cells were incubated with rhein for 1 h and then subjected to hypoxia for 6 h, followed by reoxygenation for 2 h. Cells viability, apoptosis and ROS were assayed for the treated cells. AKT, p-AKT, GSK3β, p- GSK3β, P38 and p-P38 proteins were analyzed using Western blotting. PI3K/AKT inhibitor, LY294002, and GSK3β siRNA were also used to determine the signaling pathways involved in the protection by rhein.
Results: Rhein increased viability, decreased apoptosis and ROS production, of the cells that were exposed to H/R. Rhein also increased the phosphorylation of AKT and GSK3β, an effect that was eliminated by LY294002. GSK3β silencing by siRNA showed similar effect as LY294002. The p-P38 level was upregulated by H/R and downregulated in the presence of rhein; however, the p-P38 downregulation was completely abolished by GSK3β silencing.
Conclusion: Rhein protects myocardial H9c2 cells against hypoxia/reoxygenation induced injury via AKT/ GSK3β/p38 pathway.
Keywords: H9c2 cells; Hypoxia/reoxygenation; Myocardial cells; PI3K/AKT; Rhein.
Copyright © 2018. Published by Elsevier GmbH.