| Summary: | 碩士 === 馬偕醫學院 === 生物醫學研究所 === 102 === Objective–
We studied the effect of nicotine on human late endothelial progenitor cells (EPCs)
Methods and Results -
we isolated, cultured and characterized the late EPCs from peripheral blood mononuclear cells (PBMCs) of healthy donors, and further evaluated the cellular function of migration, proliferation, and angiogenesis after treatment with different concentrations of nicotine (0.6, 6, 60, and 600 umol/L). The results showed that migration, proliferation, and angiogenesis of late EPCs were all increased by nicotine (6, 60, and 600 umol/L), and the nicotine-induced functional enhancement could be inhibited by mecamylamine (MCA), a specific inhibitor of nicotinic acetylcholine receptors (nAChRs). In hindlimb ischemia mice, we detected subcutaneous blood flow by Laser Doppler perfusion imaging every 7 days till 28 days after ligation of right femoral artery and the results showed that the perfusion was best recovered in the group of intraperitoneal infusion of nicotine (IPN; 0.01 ug/day) plus intramuscular injection of late EPCs (IMEPCs), followed by the group of IPN (0.01 ug/day) plus intramuscular saline or intraperitoneal phosphate-buffered saline (PBS) plus IMEPCs, leaving the group of untreated animals the worst results (P<0.05).
Conclusion-
exogenous nicotine augments the migration, proliferation, and angiogenesis of human late EPCs in vitro. Co-administration of low concentration nicotine (0.01 ug/day) and the late EPCs enhances the therapeutic angiogenesis of the EPCs in ischemic tissues in vivo.
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