新生小鼠缺氧缺血脑组织基质细胞衍生因子1α的表达及其作用

Expression of stromal cell derived factor-1α and its effects in hypoxic-ischemic brain tissue of neonatal mice

目的观察基质细胞衍生因子1α(SDF-1α)在新生小鼠缺氧缺血性脑组织中的表达模式,及外源性给予SDF-1α对新生小鼠脑组织增殖细胞相关核抗原ki67表达和小鼠神经行为学的影响。方法将90只KM小乳鼠分为空白组、缺氧缺血性脑损伤模型组(HIBD模型组)和SDF-1α组,每组30只。HIBD模型组和SDF-1α组于HIBD造模后30 min分别腹腔注射0.9%Na Cl和SDF-1α(每只小鼠2.0μg/d),3个亚组分别连续腹腔注射1、3、7 d,空白组仅腹腔注射等体积0.9%Na Cl。通过免疫荧光与Real-time PCR观察HIBD后不同时间点SDF-1α的表达情况,通过免疫荧光及Western blotting观察ki67的表达,通过高架十字迷宫实验观察小鼠神经行为学的变化。结果 HIBD模型组脑组织SDF-1α表达上调,第3天达高峰,与空白组相比,差异有统计学意义(P<0.01)。SDF-1α组ki67在各时间点的表达均较HIBD模型组增加(P≤0.01),小鼠的神经行为学表现也较HIBD模型组明显改善(P<0.05)。结论 SDF-1α在脑组织缺氧缺血损伤后表达上调且有时间窗。外源性SDF-1α可促进ki67的表达,对发生缺氧缺血性脑损伤的小鼠的神经行为学表现有改善作用。

Objective To explore the expression of stromal cell derived factor-1α（ SDF-1α） in the brain of mice after hypoxic ischemic brain damage（ HIBD）,and to discuss the effects of SDF-1α on the expression of ki67 and the improvement of neurological behavior. Methods Ninety KMnewborn mice were devided into blank control group,HIBD model group and SDF-1α group,with 30 mice in each group. HIBD model group and SDF-1α group were intraperitoneal injected with 0. 9% Na Cl and SDF-1α（ 2. 0 μg / d in each group） respectively at 30 min after HIBD modeling.Three subgroups were intraperitoneal injected with SDF-1α for 1,3,7 d,while blank control group were injected with equivalent 0. 9% Na Cl. SDF-1α expression at different time points were observed by immunofluorescence and Realtime PCR. ki67 expression was observed by immunofluorescence and Western blotting. Neurobehavioral improvement were recorded by elevated plus maze. Results SDF-1α expression in HIBD model group increased and reached a peak on the third day,and the difference between this group and blank control group was statistically significant（ P〈0. 01）.ki67 expression significantly increased in SDF-1α group,compared with that in HIBD model group（ P≤0. 01）. Theneurological behavior of mice in SDF-1α group also was improved,compared with HIBD model group（ P〈0. 05）.Conclusion SDF-1α expression is upregulated in HIBD model group,and reaches a peak on the third day. Exogenous SDF-1α induces the expression of ki67,and improves the learning ability of mice with HIBD.