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目的:观察垂体腺苷环化酶激活肽(pituitaryadenylatecyclase-activatingpolypeptide,PACAP)对缺血再灌注脑神经元凋亡的防治作用。方法:利用四血管结扎法,建立老龄大鼠脑缺血再灌注模型,侧脑室注射PACAP,观察脑组织丙二醛(MDA)含量和超氧化物歧物酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性,计数海马CA1区存活和凋亡神经元数目,电镜观察神经元的超微结构变化。结果:PACAP治疗后脑组织MDA含量为(1.35±0.39)nmol/mg,SOD和GSH-Px活性分别为(115±20)NU/mg、(10.3±2.0)U/mg,与缺血再灌注组有明显差异(P<0.05),海马CA1区存活和凋亡神经元数目为48.8±4.3,14.3±2.9,能促进神经元存活和减轻凋亡损伤(P<0.01),保护超微结构。结论:PACAP的保护作用可能与其降低脑组织氧自由基水平,提高抗氧化酶活性,防止神经元凋亡有关。
Objective: To observe the preventive and therapeutic effects of pituitary adenylyl cyclase-activating polypeptide (PACAP) on neuronal apoptosis induced by cerebral ischemia-reperfusion. Methods: The model of cerebral ischemia-reperfusion in aged rats was established by four-vessel ligation. PACAP was injected into the lateral ventricle to observe the content of malondialdehyde (MDA) and superoxide dismutase (SOD), glutathione Oxidase (GSH-Px) activity was measured. The number of surviving and apoptotic neurons in hippocampal CA1 region was counted. The ultrastructural changes of neurons were observed by electron microscope. Results: After treatment of PACAP, the content of MDA in brain tissue was (1.35 ± 0.39) nmol / mg and the activity of SOD and GSH-Px were (115 ± 20) NU / mg and (10.3 ± 2.0) U / (P <0.05). The number of surviving and apoptotic neurons in hippocampal CA1 area was 48.8 ± 4.3 and 14.3 ± 2.9, which could promote neuron survival and alleviate apoptosis (P <0.01) and protect the ultrastructure. CONCLUSION: The protective effect of PACAP may be related to its reduction of oxygen free radical in brain tissue, antioxidase activity and neuronal apoptosis.