Surgical flaps are frequently affected by ischemia/reperfusion (I/R) injury. Calcium-sensing receptor (CaSR) and stromal cellderived\nfactor-1�±) are closely associated with myocardial I/R injury.This study was performed to evaluate the feasibility\nof applying SDF-1�± to counteract CaSR activation-mediated I/R injury in ischemic free flaps. Free flaps that underwent ischemia\nfor 3 h were equally randomized into five groups: CaCl2, NPS2143 + CaCl2, SDF-1�± + CaCl2, AMD3100 + SDF-1�± + CaCl2, and\nnormal saline. The free flaps were harvested to evaluate flap necrosis and neovascularization after 2 h or 7 d of reperfusion. p-\nCaSR/CaSR was extensively expressed in vascular endothelial cells of free flaps after I/R injury, andactivation of the SDF-1�± /CXCR4\naxis and NPS2143 could reduce the expression of cleaved caspase-3, caspase-9, FAS, Cyt-c, and Bax and increase Bcl-2 expression;\nthe opposite was true after CaSR activation. Interestingly, initiation of the SDF-1�± /CXCR4 axis might abrogate CaSR activationinduced\nI/R injury through enhancement of microvessel density. In conclusion, CaSR might become a novel therapeutic target of\nfree flaps affected by I/R injury. Activation of the SDF-1�±/CXCR4 axis and NPS2143 could counteract CaSR activation-mediated\nI/R injury and promote free flap survival through inhibition of caspase-3/caspase-9-related cell apoptosis and enhancement of\nneovascularization.
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