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目的:研究N-甲基-D-天冬氨酸受体(NMDAR)亚单位2B(NR2B)特异性拮抗剂(Ro 25-6981)对缺氧缺血性脑损伤(HIBD)新生大鼠脑室下区(SVZ)神经干细胞(NSCs)增殖的影响。方法:7 d龄新生SD大鼠随机分为Ro 25-6981组(HIBD前2 h,腹腔注射Ro 25-6981 10 mg.kg-1)、HIBD组(HIBD前2 h,腹腔注射等剂量生理盐水)和假手术组(仅游离右侧颈总动脉,不结扎)。采用免疫组化学染色检测SVZ Nestin表达量及BrdU阳性细胞数的变化。结果:HIBD组12h后Nestin表达量开始增多,48 h达峰值,之后缓慢下降;与其相比,Ro 25-6981组在12 h和24 h时下降明显(P<0.05)。HIBD组BrdU阳性细胞数在缺氧缺血3 h后缓慢上升,72 h达高峰;与其相比,Ro 25-6981组在各时间点BrdU阳性细胞表达均有所下降,以24、48和72 h减少明显,尤以72 h为著(P<0.05)。结论:Ro 25-6981能够降低HIBD新生大鼠SVZ Nestin的表达及Brdu阳性细胞数,对SVZ NSCs增殖起抑制作用,提示NR2B参与并促进HIBD引起的SVZ NSCs的增殖。
AIM: To investigate the effect of Ro 25-6981, a specific antagonist of 2B (NR2B), a N-methyl-D-aspartate receptor (NMDAR) subunit, on the brain of neonatal rats with hypoxic-ischemic brain damage (SVZ) neural stem cells (NSCs) proliferation. Methods: Newborn SD rats of 7 days old were randomly divided into Ro 25-6981 group (2 h before HIBD, Ro 25-6981 10 mg.kg-1), HIBD group (2 h before HIBD, intraperitoneal injection of isodose Saline) and sham-operated group (free right common carotid artery only, no ligation). The expression of SVZ Nestin and the number of BrdU positive cells were detected by immunohistochemical staining. Results: The expression of Nestin began to increase 12 h after HIBD and peaked at 48 h, then decreased slowly. Compared with that in Ro 25-6981 group, the expression of Nestin decreased significantly at 12 h and 24 h (P <0.05). The number of BrdU positive cells in HIBD group increased slowly 3 h after hypoxia-ischemia and peaked at 72 h. Compared with that in Ro 25-6981 group, the expression of BrdU positive cells decreased at 24, 48 and 72 h decreased significantly, especially for 72 h (P <0.05). Conclusion: Ro 25-6981 can reduce the expression of SVZ Nestin and the number of Brdu-positive cells in neonatal rats with HIBD, which can inhibit the proliferation of SVZ NSCs. It suggests that NR2B is involved in and promotes the proliferation of SVZ-NSCs induced by HIBD.