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目的:研究灯盏花素对大鼠脑缺血-再灌注引起脑损伤的保护作用,探讨其作用机制。方法:雄性Wistar大鼠40只,随机分成5组:假手术组、模型组、MgSO4阳性对照组、灯盏花素低、高剂量组。假手术组、模型组于脑缺血-再灌注10min后给予20mL/kg生理盐水,其余3组给予50、75mg/kg灯盏花素及30mg/kgMgSO4。用TUNEL法和免疫组化法分别检测脑组织凋亡细胞和NF-κB阳性细胞的变化。结果:MgSO4组、Bre高、低剂量组在脑缺血-再灌注23h后海马区凋亡神经元/海马神经元分别为(35.4±5.5)%,(27.2±4.3)%和(20.6±3.6)%,均较模型组海马区凋亡神经元/海马神经元(60.4±6.2)%为低,但Bre组比MgSO4组凋亡细胞更低,差异具有显著性意义。MgSO4组、Bre高、低剂量组在脑缺血-再灌注23h后海马区NF-κB表达阳性神经元/海马神经元分别为(45.2±4.2)%、(32.1±5.3)%和(19.5±3.5)%,均较模型组海马区NF-κB表达阳性神经元/海马神经元(73.1±6.2)%为低,但Bre组比MgSO4组凋亡细胞更低,差异具有显著性意义。结论:灯盏花素可显著保护大脑缺血-再灌注引起的脑损伤,可能与其抑制NF-κB蛋白的表达有关。其作用优于单用MgSO4。
Objective: To study the protective effect of Breviscapine on brain injury induced by cerebral ischemia-reperfusion in rats and to explore its mechanism of action. METHODS: Forty male Wistar rats were randomly divided into 5 groups: sham operation group, model group, MgSO4 positive control group, and low-dose high-dose breviscapine group. In the sham operation group and the model group, 20 mL/kg physiological saline was administered 10 min after cerebral ischemia-reperfusion, and the other three groups were given 50, 75 mg/kg breviscapine and 30 mg/kg MgSO4. The changes of apoptotic cells and NF-κB positive cells in brain tissue were detected by TUNEL and immunohistochemistry, respectively. RESULTS: Apoptotic neurons/hippocampal neurons in hippocampus of MgSO4 group, Bre high and low dose groups were (35.4±5.5)%, (27.2±4.3)% and (20.6±3.6), respectively, after cerebral ischemia-reperfusion for 23h. The percentage of apoptotic neurons/hippocampal neurons in the hippocampus of the model group was lower than that of the model group (60.4±6.2)%, but the Bre cells in the Bre group were lower than the MgSO4 group, and the difference was significant. The expression of NF-κB-positive neurons/hippocampal neurons in hippocampus of MgSO4 group and Bre high-dose group was (45.2±4.2)%, (32.1±5.3)%, and (19.5±) respectively after cerebral ischemia-reperfusion for 23h. 3.5)% were lower than the NF-κB positive neurons/hippocampal neurons in the hippocampus of the model group (73.1 ± 6.2)%, but the Bre cells in the Bre group were lower than the MgSO4 group. The difference was significant. CONCLUSION: Breviscapine can significantly protect brain damage induced by cerebral ischemia-reperfusion, which may be related to its inhibition of NF-κB protein expression. Its role is better than using MgSO4 alone.