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目的 7日龄新生大鼠短暂脑缺血诱导侧脑室室管膜下区(SVZ)神经干细胞增殖,观察胰岛素样生长因子1(IGF-1)对神经干细胞增殖的影响。方法 7日龄新生SD大鼠64只,随机分为缺血组(n=24)、假手术组(n=24)、缺血阻断剂组(n=8)和缺血生理盐水组(n=8)。利用免疫组织化学方法观察缺血组和假手术组在缺血后1、4、7d SVZ新生细胞数量和IGF-1表达的变化,并观察缺血阻断剂组和缺血生理盐水组在IGF-1受体阻断剂(JB1)阻断7d后SVZ新生细胞数量和IGF-1表达的变化。结果与同时间点假手术组比较,缺血后1、4、7d的SVZ新生细胞和IGF-1阳性细胞数量均显著增加,差异有统计学意义(P<0.05);使用JB1后,缺血阻断剂组IGF-1的表达被阻断,IGF-1阳性细胞缺如,而缺血生理盐水组IGF-1表达正常;使用JB1后,缺血阻断剂组SVZ新生细胞数量显著减少,与缺血生理盐水组相比,差异有统计学意义(P<0.05)。结论新生大鼠缺血再灌注损伤上调了IGF-1的表达,IGF-1表达增加促使SVZ神经干细胞增殖;使用JB1后,IGF-1的表达被阻断,神经干细胞增殖也显著减少,提示IGF-1在脑缺血损伤修复中起关键作用。
Objective To observe the effect of insulin-like growth factor 1 (IGF-1) on the proliferation of neural stem cells (SVZ) induced by transient cerebral ischemia in 7-day-old neonatal rats. Methods Sixty-four SD neonatal SD rats (7 days old) were randomly divided into ischemia group (n = 24), sham operation group (n = 24), ischemia blocker group (n = 8) and ischemia NS group n = 8). Immunohistochemistry was used to observe the number of SVZ neovascularization cells and the expression of IGF-1 in ischemic group and sham operation group at 1, 4 and 7 days after ischemia. The changes of IGF- -1 receptor blocker (JB1) blocked the number of SVZ neonate cells and IGF-1 expression after 7 days. Results Compared with the sham group, the numbers of SVZ neutrophil and IGF-1 positive cells at 1, 4 and 7 days after ischemia increased significantly (P <0.05). After using JB1, ischemia The expression of IGF-1 in the blocker group was blocked, the IGF-1 positive cells were absent, while the IGF-1 expression was normal in the ischemic saline group. After administration of JB1, the number of SVZ neonate cells in ischemic blockers decreased significantly, Compared with ischemic saline group, the difference was statistically significant (P <0.05). CONCLUSION: Ischemia-reperfusion injury can up-regulate the expression of IGF-1 in neonatal rats and increase the expression of IGF-1 to promote the proliferation of SVZ neural stem cells. After using JB1, the expression of IGF-1 is blocked and the proliferation of neural stem cells is significantly reduced. -1 plays a key role in the repair of cerebral ischemia.