加减薯蓣丸抑制单磷酸腺苷活化蛋白激酶活性对慢性脑灌注不足大鼠的神经保护研究

目的 检测慢性脑灌注不足大鼠海马组织单磷酸腺苷活化蛋白激酶（adenosine monophosphate-activated protein kinase, AMPK）水平的变化，探讨加减薯蓣丸对海马神经细胞损伤的影响及其作用机制。方法 采用改良双侧颈总动脉阻断法复制慢性脑灌注不足模型，应用尼氏染色检测神经细胞损伤情况，应用Western blot法检测海马区AMPK及p-AMPK表达水平。结果 与正常组比较，模型组大鼠海马CA1区的尼氏染色较浅，神经锥体细胞数减少，海马组织p-AMPK表达水平明显升高（P<0.05）；与模型组比较，中药组与西药组大鼠海马CA1区的尼氏染色加深，锥体细胞数量增加，p-AMPK表达水平明显下降（P<0.05）；中药组与西药组大鼠海马CA1区AMPK和p-AMPK表达水平比较，差异均无统计学意义（P>0.05）。结论 大鼠慢性脑灌注不足损伤后，AMPK过度激活，出现海马神经细胞损伤，加减薯蓣丸可抑制海马区AMPK的激活，减轻海马神经损伤。

Neuroprotective Effect of Modified Dioscorea opposita Thunb. Pill on Rats with Chronic Cerebral Hypoperfusion by Inhibiting the Activity of Adenosine Monophosphate-activated Protein Kinase

Objective To investigate the change in adenosine monophosphate-activated protein kinase (AMPK) in the hippocampal tissue of rats with chronic cerebral hypoperfusion and the effect of modified Dioscorea opposita Thunb. Pill on hippocampal nerve cell damage and related mechanisms of action. Methods Modified bilateral common carotid artery occlusion was performed to establish a rat model of chronic cerebral hypoperfusion. Nissl staining was used to observe nerve cell damage, and Western blot was used to measure the expression of AMPK and phosphorylated AMPK (p-AMPK) in the hippocampus. Results Compared with the normal group, the model group had a significantly lighter color of Nissl staining, a significant reduction in the number of pyramidal cells, and a significant increase in the expression of p-AMPK in the hippocampal CA1 region (P<0.05). Compared with the model group, the traditional Chinese medicine group and the Western medicine group had a significantly darker color of Nissl staining, a significant increase in the number of pyramidal cells, and a significant reduction in the expression of p-AMPK in the hippocampal CA1 region (P<0.05). There were no significant differences in the expression of AMPK and p-AMPK in the hippocampal CA1 region between the traditional Chinese medicine group and the Western medicine group (P>0.05). Conclusion Excessive activation of AMPK after chronic cerebral hypoperfusion in rats causes hippocampal nerve cell damage, and modified Dioscorea opposita Thunb. Pill can inhibit the activation of AMPK and alleviate nerve injury in the hippocampus.