Prazosin blocks apoptosis of endothelial progenitor cells through downregulating the Akt/NF-κB signaling pathway in a rat cerebral infarction model.

ABSTRACT: Endothelial progenitor cells (EPCs) can enhance the recanalization of thrombosis during the progression of cerebral infarction. Prazosin plays a therapeutic role in expanding the peripheral vasculature and regulating infarction cardiosclerosis by inhibiting phosphoinositide signaling. However, the possible mechanisms underlying the therapeutic effects of prazosin have not been fully explored. The purpose of the present study was to analyze the anti-apoptotic effects of prazosin on EPCs in a rat cerebral infarction model. The results showed that prazosin treatment decreased apoptosis of EPCs. Prazosin treatment decreased the serum expression levels of the inflammatory factors, interleukin-1β and tumor necrosis factor-α in rats with cerebral infarctions as well as in EPCs in vitro. In

SUBMITTER: Liu S 

PROVIDER: S-EPMC7401792 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature