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目的探讨姜黄素(Curcumin)对慢性脑缺血大鼠脑组织海马CA1区损伤的修复作用及其机制。方法采用双侧颈总动脉永久性结扎建立慢性脑缺血大鼠模型,术后24 h,将模型大鼠随机分为单纯缺血组、姜黄素高剂量(100 mg/kg)治疗组和姜黄素低剂量(50 mg/kg)治疗组,另设假手术对照组和正常对照组。姜黄素高、低剂量治疗组分别经腹腔注射100和50 mg/kg姜黄素,单纯缺血组、假手术组和正常对照组腹腔注射等量的DMSO,每天1次,连续14 d。给药14 d后,取各组大鼠脑组织,HE染色和尼氏染色观察海马CA1区的形态学变化,免疫组化法观察海马CA1区神经胶质微丝酸性蛋白(Glial fib-rillaryacidic protein,GFAP)和巢蛋白(Nestin)的表达。结果与假手术组相比,单纯缺血组大鼠海马CA1区锥体细胞和尼氏小体丢失,细胞核固缩,星形胶质细胞肥大并大量增生;经姜黄素治疗后,神经元损伤明显减轻,同时伴有GFAP和Nestin阳性细胞大量增加,姜黄素高剂量治疗组与单纯缺血组相比,差异有统计学意义(P<0.05)。结论姜黄素能显著增强慢性脑缺血大鼠脑组织海马CA1区GFAP和Nestin蛋白的表达,减轻神经元损伤,对慢性脑缺血损伤有一定的治疗作用。
Objective To investigate the effect and mechanism of curcumin on the injury of hippocampal CA1 region in rat brain after chronic cerebral ischemia. Methods The model of chronic cerebral ischemia was established by permanent ligation of bilateral common carotid arteries. The rats were randomly divided into ischemia group, high dose of curcumin (100 mg / kg) and curcumin Su-low dose (50 mg / kg) treatment group, another set of sham operation control group and normal control group. Curcumin high and low dose treatment groups were injected intraperitoneally with 100 and 50 mg / kg curcumin, pure ischemia group, sham operation group and normal control group, respectively, once a day for 14 days. After administration for 14 days, the morphological changes of hippocampal CA1 region were observed by HE staining and Nissl staining. The expression of glial fibroillary acidic protein (Glial fibroillary acidic protein) , GFAP) and Nestin. Results Compared with the sham-operation group, the pyramidal cell and Nissl body of hippocampal CA1 region of rats in the ischemia group were lost, the nuclei were pyknotic and the astrocytes were hypertrophy and hyperplasia. After curcumin treatment, the neuronal damage (P <0.05). There was a significant increase in the number of GFAP and Nestin positive cells in the high dose of curcumin treatment group compared with the ischemia group (P <0.05). Conclusion Curcumin can significantly increase the expression of GFAP and Nestin protein in the hippocampal CA1 area of the rats with chronic cerebral ischemia, reduce the damage of neurons and play a therapeutic role in the treatment of chronic cerebral ischemia.