Cellular elements of maturing brain are vulnerable to insults, which lead to neurodevelopmental defects. There are no established treatments at present. Here we examined the efficacy of selective adenosine A_2A receptor inhibitor SCH58261 to combat brain injury, particularly oligodendrocyte (OL) lineage cells, in young rats. Wistar rats (n = 24, 6.5 days old) were randomly divided into equal groups of four. The sham (SHAM) group received no treatment, the vehicle (VEHICLE) group received 0.1% dimethylsufoxide, the injury (INJ) group was exposed to oxygen-glucose deprivation insult, and the injury+SCH58261 (INJ+SCH58261) group was exposed to the insult and received 1 μM SCH58261. Immunocytochemical experiments revealed that there was a significant reduction in the populations of mature OL (MBP⁺ OLs) and immature OL precursors (NG2⁺ OPCs) in the INJ group compared to SHAM group. Furthermore, there was also a significant increase in the percent of apoptotic MBP⁺ OL and NG2⁺ OPC populations as evidenced by TUNEL assay. In addition, there was a significant reduction in the proliferation rate among NG2⁺ OPCs, which was confirmed by BrdU immunostaining. On the other hand, treatment with SCH58261 significantly enhanced survival, evidenced by the reduction in apoptotic indices for both cell types, and it is preserved the NG2⁺ OPC proliferation. Activation of adenosine A_2A receptors may contribute to OL lineage cell loss in association with decreased mitotic behavior of OPCs in neonatal brains upon injury. Future investigations assessing ability of SCH58261 to regenerate myelin will provide insights into its wider clinical relevance.

成熟的大脑的细胞成分容易受到侮辱，导致神经发育缺陷。目前尚无确定的治疗方法。在这里，我们研究了选择性腺苷A _2A受体抑制剂SCH58261对抗年轻大鼠脑损伤，特别是少突胶质细胞（OL）谱系细胞的功效。将Wistar大鼠（n = 24，6.5天大）随机分为四组，每组相等。假手术（SHAM）组未接受治疗，媒介物（VEHICLE）组接受0.1％的二甲基亚砜，伤害（INJ）组受到氧-葡萄糖剥夺侮辱，伤害+ SCH58261（INJ + SCH58261）组受到并接受1μMSCH58261。免疫细胞化学实验显示，成熟OL（MBP ⁺与SHAM组相比，INJ组的OLs和未成熟的OL前体（NG2 ⁺ OPC）。此外，通过TUNEL分析证明，凋亡的MBP ⁺ OL和NG2 ⁺ OPC群体的百分比也显着增加。另外，通过BrdU免疫染色证实了NG2 ⁺ OPC之间的增殖速率显着降低。另一方面，用SCH58261进行治疗可显着提高存活率，这是通过两种细胞类型的凋亡指数降低所证实的，并且保留了NG2 ⁺ OPC的增殖。腺苷A _2A的激活新生受体可能会导致OL谱系细胞丢失，并导致新生脑损伤后OPC的有丝分裂行为减少。评估SCH58261再生髓磷脂能力的未来研究将提供对其更广泛的临床意义的见解。