Dexmedetomidine alleviates oxygen and glucose deprivation-induced apoptosis in mesenchymal stem cell via downregulation of MKP-1

Bone marrow mesenchymal stem cell (MSC)-based therapy is a novel candidate for heart repair. But ischemia-reperfusion injury leads to low viability of MSC. Dexmedetomidine (Dex) has been found protect neurons against injury. It remains unknown if Dex could increase the MSCs under ischemia. The present study observe potential protective effect on ischemia and its underlying mechanisms. Specific mRNAs related myocardial in GEO database were selected from mRNA profiles assessed previous using microarray. most dysregulated specific ones above subject bioinformatics analysis at our laboratory. These possibly regulated apoptosis cardiomyocytes validated vitro their pre-treated with 10 μM concentration 24 h oxygen-glucose deprivation (OGD). Flow cytometry TUNEL assay carried out detect Dex-pretreated OGD. relative expressions mitogen-activated protein kinase phosphatase 1 (MKP-1) genes detected by quantitative polymerase chain reaction western blotting. Microarray data revealed that regulates MAPK activity. significantly reduced OGD, which suppressed synthesis level Beclin1 light 3 proteins. down-regulated MKP-1 expression attenuated an OGD-induced change mitogen activated (MAPK3) signaling pathway. increases MSC improves tolerance OGD association pathway, thus suggesting as strategy promoting efficacy