中文摘要：

研究新合成腺苷结构类似物B2对无血清培养所致PC12细胞损伤的保护作用,并对其机制进行初步探讨。采用放射性配基3H-MSX-2与腺苷A2A受体竞争结合法检测B2与大鼠纹状体腺苷A2A受体的亲和力;MTT法检测B2对无血清培养PC12细胞存活率的影响;用荧光探针DCFDA检测细胞内活性氧（ROS）含量变化。放射性配基受体竞争结合实验求得B2与大鼠脑纹状体A2A受体结合的Ki值为0.37μmol.L 1。B2（0.1、1、10和100μmol.L 1）可使去血清培养24 h的PC12细胞存活率由模型组的49.6%分别上升至63.3%、74.9%、86.3%、88.1%。合并使用0.1μmol.L 1 SCH 58261使B2（0.1～10μmol.L 1）的作用分别下降16.1%,24.0%和19.8%。去血清培养24 h使PC12细胞内ROS含量升高为对照组的3.5倍,B2（1～100μmol.L 1）可使胞内荧光强度分别降低为对照组的3.1倍、2.4倍和1.5倍。B2对无血清培养所致PC12细胞损伤有明显的保护作用,该作用与腺苷A2A受体相关,同时可显著降低去血清培养时细胞内活性氧自由基的过度生成,可能是其产生保护作用的机制之一。

英文摘要：

This study is to investigate the effect of compound B2 on the damage of PC12 cells induced by serum deprivation and to explore its related mechanisms.The binding characteristics of B2 to rat striatum adenosine A2A receptor was studied by radioligand 3H-MSX-2 binding assay.Cell viability was detected by MTT assay.ROS formation was measured after DCFDA fluorescent staining.B2 has affinity to rat adenosine A2A receptor（Ki = 0.37 μmol L 1）.B2 remarkably increased PC12 cell survival rate in serum deprivation-induced PC12 cells.The percentage of serum deprivation-induced death of PC12 was 49.6%,and the treatment of B2（0.1 100 μmol L 1） increased the cell viability to 63.3%,74.9%,86.3% and 88.1%,respectively.Adenosine A2A receptor antagonist SCH 58261 could significantly block the protective effect of B2.The cell viability with 0.1 μmol L 1 SCH 58261 decreased by 16.1%,24.0% and 19.8%,in the presence of B2（0.1 10 μmol L 1）.Serum deprivation-induced ROS formation was 3.5 times more than that of control group,and treatment with B2 significantly and dose-dependently inhibited ROS over-formation.The protective effect of B2 may be related with adenosine A2A receptor.Decrease of serum-deprivation induced ROS formation may also be one of the mechanisms.