血管瘤组织中β肾上腺素能受体的密度及亲和力

Density and Affinity of β-adrenergic Receptors in Hemangiomas

目的研究血管瘤组织中β肾上腺素能受体(β-AR)的密度和亲和力,并探讨其在血管瘤发病中的意义。方法采用放射标记的非选择性β-AR阻滞剂125I-吲哚洛尔、选择性β1-AR阻滞剂阿替洛尔,对12例增生期血管瘤组织和10例退化期血管瘤组织的β-AR进行双位点竞争结合实验,并根据双位点数学模型,测算出增生期血管瘤和退化期血管瘤组织中的β1-AR及β2-AR的密度和亲和力(抑制常数)。结果增生期血管瘤和退化期血管瘤组织中均存在高亲和力的β1-AR和低亲和力的β2-AR。增生期血管瘤组织中β1-AR的亲和力(0.26±0.09nmol/L)和β2-AR的亲和力(2.94±0.31nmol/L)分别与退化期相比(0.27±0.06nmol/L,2.91±0.53nmol/L),差异均无统计学意义(均P>0.05)。增生期血管瘤组织中β1-AR的密度(47.31±7.76 fmol/mg protein)和β2-AR的密度(172.21±30.56fmol/mg protein)分别高于退化期(24.09±5.17fmol/mg protein,73.48±13.34fmol/mg protein),且均有统计学意义(均P<0.01)。结论血管瘤组织中存在β1-AR和β2-AR,且以β2-AR为主;增生期血管瘤组织中β1-AR和β2-AR的密度明显上调而亲和力无明显变化;血管瘤的增生可能与其β1-AR和β2-AR尤其是β2-AR的密度上调有关。

Objective To investigate the density and affinity of β-adrenergic receptors（β-AR） in hemangiomas,and to explore their role in the development of hemangiomas. Methods Dual site competitive binding assay was performed with non-selective β-AR antagonist^125 I-pindolol and β1-selective antagonist atenolol. The density and affinity（ inhibition constant,KI） of β1-AR and β2-AR in 12 proliferating hemangiomas and 10 involuted hemangiomas were detected and calculated by dual site mathematical models. Results The presence of β1-AR with high affinity and β2-AR with low affinity showed both in proliferating hemangiomas and in invo- luted hemangiomas. There was no significant difference between KI of β1-AR（0.26 ± 0.09nmol/L） in prolif- erating hemangiomas and that （0.27 ± 0.06nmol/L） in involuted hemangiomas （P 〉 0.05 ）. Similarly, no obvious difference was observed between KI of β2-AR （2.94 ± 0, 31nmol/L） in proliferating hemangiomas and that （2.91 ± 0.53 nmol/L） in involuted hemangiomas （P 〉 0.05 ）. The density of β1-AR （47.31 ± 7.76 fmol/mg protein） and β2-AR（ 172.21 ± 30.56fmol/mg protein） in proliferating hemangiomas were respectively higher than those （24.09 ± 5.17fmol/mg protein, 73.48 ±13.34fmol/mg protein） in involuted heman- giomas（P〈0.01,respectively）. Conclusion There exist β1-AR and β2-AR（β2-AR predominate） in he- mangiomas. There is significant up-regulation in density of β1-AR and β2-AR in proliferating hemangiomas while there is no obvious change in affinity of these β-AR subtypes. The up-regulated density of β1-AR and β2-AR（β2-AR predominate） in proliferating hemangiomas may be related with hemangiomatous proliferation.