缺血/再灌注小鼠海马组织cAMP和腺苷环化酶mRNA水平的变化

目的:观测缺血/再灌注小鼠海马组织环磷酸腺苷(cAMP)和腺苷环化酶(AC)mRNA水平,探讨缺血/再灌注发病的分子生物学机制.方法:通过双侧颈总动脉线结、连续3次缺血-再灌注,制作缺血/再灌注动物模型,并设立假手术组;术后29 d、30 d分别测试学习和记忆成绩;应用放射免疫法检测小鼠海马组织cAMP水平,应用原位杂交技术检测ACmRNA水平.结果:与假手术组比较,模型组学习和记忆成绩均降低(P＜0.05),且海马组织cAMP水平也降低(P＜0.05),海马CA1区AC mRNA阳性神经元面密度明显降低(P＜0.05).结论:海马组织cAMP和AC mRNA水平降低可能参与了缺血/再灌注后学习和记忆障碍的分子生物学发病机制.

The changes of cAMP and adenylyl cyclase mRNA level in hippocampus of mice with ischemia/reperfusion

To observe the cAMP and adenylyl cyclase(AC) mRNA level in hippocampus of mice with vascular dementia(ischemia/reperfusion), and explore the molecular pathogenesis of ischemia/reperfusion. Methods: The mice were subjected for ischemia/reperfusion three times on bilateral common carotid arteries by knots to establish models of ischemia/reperfusion and the changes of learning and memory were tested on 29 d/30 d after operation. Shamed-operation mice were introduced as control group. The cAMP level was evaluated by the radioimmunoassay(RIA), AC mRNA positive neurons of hippocampus CA1 area were dyed through in-situ hybridization(ISH). Results: Compared with shamed-operation group, the learning and memory of model group was worse(P<(0.05)), the cAMP level in hippocampus was lower(P<(0.05)) and the surface density(Sv) of AC mRNA positive neurons reduced(P<(0.05)). Conclusion: The lower cAMP and AC mRNA level in hippocampus might participate in the molecular pathogenesis of ischemia/reperfusion.