目的 探讨当归多糖(APS)对脑缺血再灌注损伤大鼠海马神经元的保护作用.方法 将50只大鼠随机分为假手术组、模型组和APS高、中、低剂量(200、100、50 mg/kg)组,APS给药组于造模前3 d连续ig给予APS,假手术组和模型组ig等量生理盐水;采用线栓法制备大鼠脑缺血再灌注损伤(I/R)模型,缺血2 h、再灌注24 h后,跳台法检测大鼠学习记忆能力,TUNEL法检测大鼠海马神经元凋亡情况,ELISA法检测海马组织中cleaved caspase-3、bcl-2及bax的表达.结果 与假手术组相比,模型组大鼠跳台潜伏期明显缩短,错误次数增加,神经元凋亡率增加,cleaved caspase-3、bcl-2及bax的表达显著升高.与模型组相比,APS各剂量组大鼠跳台潜伏期明显延长,错误次数减少,并降低了神经元凋亡率,减少cleaved caspase-3及bax的表达,且增加bcl-2表达.结论 APS对I/R大鼠具有明显的神经保护作用,其机制可能与抑制神经元凋亡密切相关.

Objective To investigate the protection of angelica polysaccharide (APS) on hippocampal neuron in rats with cerebral ischemia-reperfusion (I/R) injury. Methods The model of cerebral I/R injury was established by suture method in rats. A total of 50 rats were randomly divided into five groups: Sham-operation, cerebral I/R injury, high-dose APS (200 mg/kg), mid-dose APS (100 mg/kg), and low-dose APS (50 mg/kg) groups. APS was ig administrated 3 d before operation. At 24 h after reperfusion, learning and memory function was detected by step down test, the apoptosis of hippocampal neuron was observed by terminal deoxylnucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), and the expression of cleaved caspase-3, bcl-2, and bax in the hippocampus of rats was measured by enzyme-linked immunosorbent assay (ELISA). Results Compared with those in the Sham-operation group, the learning and memory function was notably impaired in the I/R injury group, the number of errors increased. The apoptosis of hippocampal neuron increased and the expression of cleaved caspase-3, bcl-2, and bax in the hippocampus remarkably increased in the I/R injury group. The APS could significantly improve the learning and memory function of rats with the cerebral I/R injury and remarkably delay the decrease of the number of errors and the decrease of the apoptosis rate in the hippocampus of rats with the cerebral I/R injury. And the APS could also cause a significant down-regulation of cleaved caspase-3 and bax expression, while up-regulation of bcl-2 expression in hippocampus of rats with the cerebral I/R injury. Conclusion APS has a neuroprotection on rats with the cerebral I/R injury. The neuroprotective mechanism of APS may involve in the inhibition of the neuronal apoptosis.