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目的探讨黄芪多糖(Astragalus Polysaccharide,APS)对大鼠蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后早期脑损伤(Early brain injury,EBI)的保护作用及其机制。方法根据随机数据表法将100只大鼠随机分为4组,每组25只,即假手术组(Sham组)、SAH组、赋形剂对照组(Vehicle组)和APS组。在SAH后1 h和6 h,APS组腹腔注射APS溶液(10 mg·kg~(-1),3 mL),vehicle组注射相同体积的生理盐水,其他组不做任何处理。观察各组大鼠死亡率、SAH等级、神经功能和脑水肿情况,同时,进行生化实验和组织学研究。结果死亡率调查结果显示,Sham组中大鼠无死亡,SAH组、Vehicle组和APS组的死亡率依次为20.0%(5/25)、16.0%(4/25)和20.0%(5/25)。经APS治疗后,APS组的神经功能和脑含水量较Vehicle组和SAH组显著改善(P<0.05)。免疫组化和Western blot分析结果均显示,SAH大鼠经APS治疗后p-Akt、p-Bad蛋白表达较SAH组和Vehicle组显著提高(P<0.05),同时Caspase-3蛋白表达显著降低(P<0.05)。结论 APS可通过抗凋亡作用减轻SAH后的EBI,并保护神经元细胞,其作用机制可能与调节PI3K/Akt通路有关。
Objective To investigate the protective effect of astragalus polysaccharide (APS) on early brain injury (EBI) after subarachnoid hemorrhage (SAH) in rats and its mechanism. Methods 100 rats were randomly divided into 4 groups (n = 25), sham operation group (Sham group), SAH group, vehicle control group and APS group. APS solution (10 mg · kg -1, 3 mL) was intraperitoneally injected into the APS group 1 h and 6 h after SAH, and the same volume of saline was injected into the vehicle group. The rats in the other groups were given no treatment. The mortality, SAH level, neurological function and brain edema were observed in each group. At the same time, biochemical experiments and histological studies were performed. Results There was no death in the Sham group. The mortality rates in the SAH, Vehicle and APS groups were 20.0% (5/25), 16.0% (4/25) and 20.0% (5/25), respectively ). After APS treatment, the neurological function and brain water content in APS group were significantly improved compared with vehicle group and SAH group (P <0.05). The results of immunohistochemistry and Western blot showed that the expression of p-Akt and p-Bad protein in SAH rats was significantly increased (P <0.05) compared with SAH group and vehicle group, and the expression of Caspase-3 protein was significantly decreased P <0.05). Conclusions APS can reduce the EBI after SAH by anti-apoptosis and protect the neuronal cells. Its mechanism may be related to the regulation of PI3K / Akt pathway.