摘要
目的探讨CCR5亲和短肽对单核细胞趋化活性的影响。方法采用流式细胞仪观察短肽对单抗2D7与单核细胞结合的影响;QuantikineHumanRANTES试剂盒检测短肽与RANTES对单核细胞的竞争性结合作用;体外趋化性实验观察短肽对单核细胞的趋化作用;大鼠体内实验观察短肽对动脉粥样硬化形成的影响。结果短肽能抑制2D7与单核细胞的结合;也能竞争性抑制RANTES与单核细胞的结合,其IC50约为5.6mgL(3.98μmolL)。在体外,短肽对单核细胞没有趋化性(P=0.074),且能抑制RANTES对单核细胞的趋化作用,短肽+RANTES组的穿膜细胞数(23±10)显著少于RANTES组(62±13)。体内实验结果表明,短肽能降低单核细胞在大鼠主动脉弓部位的聚集(P<0.05)。结论短肽对单核细胞具有很强的亲和作用,且短肽能抑制单核细胞对RANTES的趋化性,因而可降低或延缓动脉粥样硬化进程。
Aim To investigate the effects of peptide specific to CCR5 on monocyte chemotaxis, Methods The effects of peptide on the binding of mAb 2D7 to monocyte were surveyed by flow cytometry; Competitive binding of peptide and RANTES on monocyte was measured through Quantikine Human RANTES kit; Chemotaxis assay of monocyte toward peptide was performed in vitro;Effects of peptide on atheroselerosis formation was detected in vivo in mice, Results Peptide could inhibit the binding of 2D7 and RANTES to monocyte (IC50 was about 3,98μmol/L). Invitro, peptide showed no chemotactic effect to monocyte( P = 0.074) and could inhibit chemotaetic activity of monocyte toward RANTES, the cell number of migration in the peptide + RANTES groups (23 ± 10) was lower than that of the RANTES groups (62 ± 13), Peptide could impair the influx of monocyte to the aortic root in mice( P 〈 0.05). Condusion Peptide could target to monocyte and suppress chemotactic activity of monocyte toward RANTES and reduce atherosclerosis.
出处
《中国动脉硬化杂志》
CAS
CSCD
2006年第5期399-401,共3页
Chinese Journal of Arteriosclerosis
基金
湖南省教育厅科学研究基金项目(00C156)资助