灯盏乙素抗新生大鼠缺氧缺血性脑损伤的作用及对p38 MAPK表达的影响

Anti-injury effect of scutellarin on the hypoxic ischemic brain damage of neonatal rats and the expression of p38 MAPK

目的探讨灯盏乙素抗新生大鼠缺氧缺血性脑损伤的作用及对p38 MAPK表达的影响及机制。方法 45只健康新生7日龄SD大鼠随机分为假手术组、缺血缺氧组、灯盏乙素组(25 mg/kg)。分别于用药后第24小时、3天、7天每组处死大鼠各5只,取脑组织切片。采用TUNEL染色检测神经细胞凋亡;采用免疫组织化学染色检测p38 MAPK的表达高峰、表达变化趋势。结果缺氧缺血后海马CA1区神经细胞凋亡,p38 MAPK表达增加;灯盏乙素组神经细胞凋亡及p38 MAPK表达均减少(与同一时间点缺氧缺血组比较差异有统计学意义P<0.05)。结论灯盏乙素可能是通过抑制p38MAPK信号通路而减少神经细胞凋亡,从而发挥脑保护作用。

Objective To study the effects of scutellarin treat HIBD in neonatal rats and the expression of p38 MAPK signal pathway following HIBD and its mechanism. Methods 45 healthy 7-day-old neonatal SD rats were randomly divided into sham operation group, HIBD group, and scutellarin group（25 mg/kg）. After medication, each group respectively executed 5 rats in 24 h, 3 d, 7 d, and took brain tissue slice. The neuronal apoptosis was detected using TUNEL assay. The highest expression and expressional tendencies of p38 MAPK was determined by the method of immunohistochemistry. Results The apoptotic neurons, actived p38 MAPK increased after HIBD in the hippocampal CA1 region. The expression level of p38 MAPK and apopotic neurons in scultellarin group were significantly lower than HIBD group （the differences of the same time point were statistically significant P〈0.05 ）. Conclusion Scultellarin could reduce the apoptosis through inhibiting the p38 MAPK signal pathway with cerebral hemorrhage.