诺迪康对大鼠脑缺血再灌注损伤的脑保护作用

Brain protective effects of Nuodikang capsule in rats with cerebral ischemia reperfusion injury

目的观察诺迪康胶囊对大鼠局灶性脑缺血冉灌注损伤神经细胞热休克蛋白70(HSP70)表达的影响。方法60只健康雄性Wistar大鼠,采用大脑中动脉线栓法建立局灶性脑缺血再灌注大鼠模型,并随机将大鼠分为假手术组、缺血再灌注组、诺迪康胶囊大、小剂量组,每组15只。诺迪康治疗组分别按0.672 g/kg(大剂量)和0.336 g/kg(小剂量),术前连续4周每天早晚两次灌胃。假手术组和缺血再灌组分别灌以10 mL/kg的生理盐水。脑缺血2 h再灌注后6 h进行神经功能缺损评分,24 h后断头取脑,采用免疫组织化学法检测脑组织中HSP70蛋白的表达,TTC染色测定脑梗死体积,并与病理组织学改变进行对照。结果大剂量诺迪康胶囊能明显增强大脑皮质及海马组织HSP70的表达,减轻神经细胞损伤,与缺血再灌注组、诺迪康小剂量组比较,P<0.05,与假手术组比较,P<0.01。结论诺迪康胶囊能减轻脑组织的缺血再灌注损伤,改善神经功能缺失,其作用机制可能与增加HSP70表达有关。

Objective To observe the effects of Nuodikang capsule on the expression of heat shock protein 70（HSP70） in nerve cells of rats with cerebral ischemia reperfusion injury. Methods Sixty healthy male Wistar rats were selected to establish focal cerebral ischemia reperfusion model by middle cerebral artery thread embolism method and were randomly divided into sham operated group, ischemia/reperfusion group, high-dose Nuodikang capsule group, and low-dose Nuodikang capsule group. There were fifteen rats in each group. Nuodikang capsule groups were given Nuodikang capsule at 0.672 g/kg and 0.336 g/kg. sham operated and ischemia/reperfusion group were given normal sodium at 10 mg/kg. The drugs were given twice a day consecutively for four weeks before operation. After 2 h ischemia and 6 h reperfusion injury, neurological deficits were measured and after 24 h reperfusion injury, the rats were killed and their brains were taken out. The HSP70 expression in brain tissue was detected by immunohistochemical method. Infarct sizes were measured with TTC staining and were compared with the changes of pathohistology. Results High-dose Nuodikang capsule could obviously increase the HSP70 expression in cerebral cortex and hippocampus and relieve nerve cell injury when compared with ischemia/reperfusion group and low-dose Nuodikang capsule group（P〈0.05）.and sham group（P 〈0.01）. Conclusion Nuodikang capsule can relieve ischemia reperfusion injury of brain tissue and improve nerve function. The mechanism may be related to the increase of HSP70 expression.