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目的:观察新生大鼠缺氧缺血性脑损伤(HIBD)后不同时间点皮层与海马胶质原纤维酸性蛋白(gial fibrillaryacidic protein,GFAP)表达情况,以及不同剂量丙酸睾酮(T)预处理后对其表达的影响,揭示丙酸睾酮对HIBD新生大鼠脑保护作用及其时间、量效关系。方法:200只3日龄SD大鼠随机分为3组,T预处理组80只、HIBD对照组80只和假手术组40只;T组和HIBD对照组再各自分为30 mg/kg组、120 mg/kg组。T组中每剂量组每只大鼠均给丙酸睾酮,HIBD对照组中每剂量组每只大鼠均给相应ml数花生油,方法同T组。7日龄时T组和HIBD对照组制作HIBD模型,对比观察HI后不同组别及各剂量组在24、48、72 h、7天和14天海马和大脑皮层GFAP表达的动态变化。结果:HIBD对照组脑组织30、120 mg/kg组GFAP的平均光密度数值均显著高于相同时间点的假手术组,其差异具有统计学意义(P<0.01)。T干预后,海马、皮层30、120 mg/kg两个剂量组GFAP的平均光密度较HIBD对照组各相同剂量组在相同时点GFAP平均光密度量显著减少,且差异有统计学意义(P<0.01)。HIBD对照组以及T组内的两个剂量组之间比较,在海马、皮层相同时间点GFAP的表达量的差异无统计学意义(P>0.05)。结论:新生大鼠HIBD后,脑组织GFAP的表达增加。T干预可抑制脑组织因HIBD所致的GFAP的过度表达,有抑制脑损伤区星形胶质细胞的过度增殖分裂,减少胶质瘢痕形成对神经轴突修复的不利影响的脑保护作用。
OBJECTIVE: To observe the expression of glial fibrillary acid protein (GFAP) in cortex and hippocampus at different time points after hypoxic-ischemic brain damage (HIBD) in neonatal rats and the effect of different doses of testosterone propionate (T) pretreatment After the impact on the expression of the testosterone propionate on HIBD neonatal rat brain protective effect and its time, dose-effect relationship. Methods: Two hundred three-day-old SD rats were randomly divided into three groups: 80 rats in T preconditioning group, 80 rats in HIBD control group and 40 rats in sham operation group. T rats and HIBD control rats were divided into 30 mg / kg group , 120 mg / kg group. Testosterone propionate was given to each rat in each dose group in T group. Corresponding ml peanut oil was given to each rat in each dose group in HIBD control group, the same way as in T group. HIBD model was made in T group and HIBD control group at 7 days of age. The dynamic changes of GFAP expression in hippocampus and cerebral cortex of different groups and different dose groups were observed at 24, 48, 72, 7 and 14 days after HI. Results: The mean optical density of GFAP in 30 and 120 mg / kg brain tissue in HIBD control group were significantly higher than those in sham operation group at the same time point (P <0.01). T, the average optical density of GFAP in hippocampus and cortex at 30,120 mg / kg dose group was significantly lower than that of HIBD control group at same time point (P <0.05), and the difference was statistically significant (P <0.01). There was no significant difference in GFAP expression between HIBD control group and T group at the same time points in hippocampus and cortex (P> 0.05). Conclusion: The expression of GFAP in brain tissue increased after HIBD in neonatal rats. T intervention can inhibit brain tissue HIBD-induced GFAP overexpression, inhibition of brain injury area astroglial hyperproliferation and division, to reduce glial scar formation on the axonal repair of the adverse effects of cerebral protection.