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[摘要]
目的 探讨血清中神经元特异性烯醇化酶(NSE)、炎性因子肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)在大鼠脑缺血损伤后的作用及嘎日迪-13对其影响。方法 取雄性SD大鼠360只,将大鼠随机分为脑缺血模型组、假手术组及嘎日迪-13大、中、小剂量(0.24、0.12、0.06 g/kg)组,每组又随机分为缺血1、6、12、24、72、120 h的6个时相组,采用改良Zea Longa线栓法制备大鼠大脑中动脉栓塞(MCAO)模型,ELISA法检测血清中NSE、TNF-α、IL-6水平。结果 NSE、TNF-α、IL-6在假手术组表达少;而在模型组脑缺血损伤1 h后开始上升,NSE于12 h达高峰,TNF-α、IL-6在24 h达高峰,之后逐渐下降(P<0.01);嘎日迪-13各剂量治疗组能显著降低神经功能评分,NSE、TNF-α、IL-6表达量明显受到抑制(P<0.01、0.05)。结论 嘎日迪-13对大鼠脑缺血损伤具有明显的保护作用,提示嘎日迪-13可能是通过减轻脑缺血损伤后神经元的损伤,调节炎症因子相互之间的作用,减轻脑组织损伤,从而发挥对脑缺血损伤的治疗作用。
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[Abstract]
Objective To investigate the roles of neuron-specific enolase (NSE), tumor necrosis factor-α(TNF-α), and interleukins-6 (IL-6) in serum on focal cerebral ischemic injury of rats as well as the effect of Gridi-13 on them. Methods A total of 360 male SD rats were selected. They were randomly divided into model group, Sham-operated group, Gridi-13 large dose group, Gridi-13 middle dose group, and Gridi-13 small dose group. Each group was randomly divided into 1, 6, 12, 24, 72, and 120 h time phase groups. The middle cerebral artery occlusion (MCAO) model was established by modified Zea Longa thread-occlusion method and the contents of NSE, TNF-α, and IL-6 in serum were determined by ELISA method. Results The expression of NSE, TNF-α, and IL-6 was very weak in Sham-operated group while rising after the cerebral ischemic injury for 1 h compared with the model group. The peak values of NSE, TNF-α, and IL-6 appeared at 12, 24, and 24 h, respectively and then going down gradually (P < 0.01). Gridi-13 in each dose group could predominantly reduce the nervous function score and the expression levels of NSE, TNF-α, and IL-6 were remarkably inhibited (P < 0.01 and P < 0.05). Conclusion Garidi-13 has the significant protection on the cerebral ischemia injury in rats, which may be related with alleviating neuronal damage, regulating inflammatory factors, and relieving the injury of brain tissue, so as to play a role of therapeutic action in cerebral ischemic injury of rats.
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[基金项目]
国家自然科学基金资助项目(81160560)