P4239
Bradykinin inhibits High Glucose-Induced Senescence of c-kit Positive Cardiac Stem Cells via B2R/PI3K/AKT/mTOR/P53 signal pathway

Extract

Introduction: Stress-induced premature senescence may lead to dysfunction of cardiac stem cells. The peptide bradykinin (BK) is a potent vasodilator and inflammatory mediator that can protect endothelial and myocardial cells against inflammation and ischemia injury via the B2 receptor (B2R). However, if BK can inhibits high- Glucose-Induced Senescence of c-kit Positive Cardiac Stem Cells is remain unknown.

Purpose: The purpose of the study is to determine the mechanism of BK inhibits High Glucose-Induced Senescence of c-kit Positive Cardiac Stem Cells

Methods: C-kit positive CSCs were cultured from C57BL/6J mouses. CSCs were exposed to 25mM D- glucose (D-Glu) with or without treatment with BK. β-galactosidase staining (SA-Gal) and dichlorofluorescein diacetate probe (DCFH-DA) were used to detect senescence and intra-cellular oxidative stress oxygen radicals. B2R antagonist HOE-140, phosphatidylinositol-3-kinase (PI3K) antagonist LY-294002, mTOR antagonist Rapamycin, P53 antagonist PFT-α and B2 receptor siRNA were administered to block the B2R, PI3K, mTOR and P53 signal pathway. Concentration of super oxide and ATP was analyzed. B2R expression of CSCs was determined by Flow cytometry. Western blot was applied to find senescence associated signal protein.