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目的探讨缺氧和(或)缺血对幼龄大鼠脑白质损伤及脑损伤后少突胶质细胞(OL)的影响。方法选择3日龄同窝生SD低龄新生大鼠128只,随机分为4组:缺氧缺血组、单纯缺血组、单纯缺氧组、对照组。建立未成熟鼠缺氧缺血脑损伤模型,采用组织切片HE染色、OL抗体O4和细胞凋亡免疫组织化学双标记方法,观察各组脑损伤新生大鼠脑组织的形态学变化。结果缺氧和(或)缺血引起幼龄大鼠脑组织损伤,以白质损伤为主,出现白质疏松和脑室扩大等病理变化,深部脑白质OL凋亡数增多(P<0.05)。缺氧或缺血单因素均可诱导OL数减少,并发生凋亡,缺氧、缺血二因素存在协同作用(P<0.01),但缺血较缺氧对新生大鼠脑OL细胞的促凋亡作用更明显,术后48h和72h效应指数分别为7.34/2.42和7.15/1.89。结论缺氧和(或)缺血均可导致脑白质损伤及OL凋亡增多,缺血较缺氧促OL凋亡更明显,缺氧缺血存在协同作用。
Objective To investigate the effects of hypoxia and / or ischemia on oligodendroglial cells (OL) in young rats with white matter damage and brain injury. Methods 128 low birth-newborn SD rats of 3 days old were randomly divided into 4 groups: hypoxic-ischemic group, ischemia-only group, hypoxia-only group and control group. The model of hypoxic-ischemic brain damage in immature mice was established. The histological changes of brain tissue in neonatal rats with brain injury were observed by HE staining, OL antibody O4 and double-labeling immunohistochemistry. Results Hypoxia and / or ischemia caused brain injury in young rats. The main pathological changes were white matter damage and ventricular enlargement. The number of OL apoptosis in deep white matter increased (P <0.05). Apoptosis, hypoxia and ischemia were associated with synergistic effects of both hypoxia and ischemia (P <0.01). However, both ischemia and hypoxia induced OL cell apoptosis in neonatal rats The effect of apoptosis was more obvious. The effect indexes at 48h and 72h after surgery were 7.34 / 2.42 and 7.15 / 1.89 respectively. Conclusion Both hypoxia and / or ischemia can lead to the increase of white matter damage and OL apoptosis. The ischemia is more obvious than hypoxia and promote the apoptosis of OL. There is a synergistic effect of hypoxia and ischemia.