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目的探讨缺血性脑损伤中HSP72对大鼠神经元的保护作用及其分子机制。方法将SD大鼠随机分为假手术组、缺血再灌注对照组、热休克处理组、HSP72反义寡核苷酸组及溶剂组。采用焦油紫染色、免疫印迹检测大鼠缺血再灌注后海马神经元损伤和脑组织AKT、Bad(Ser136)的磷酸化情况。结果热休克处理组与缺血再灌注对照组、HSP72反义寡核苷酸组和溶剂组相比海马神经元损伤减轻,脑组织AKT和Bad(Ser136)磷酸化升高(P<0.05)。结论HSP72可能通过升高脑组织中AKT和Bad(Ser136)的磷酸化程度起到海马神经元保护作用。
Objective To investigate the protective effect of HSP72 on neurons in ischemic brain injury and its molecular mechanism. Methods SD rats were randomly divided into sham operation group, ischemia reperfusion control group, heat shock treatment group, HSP72 antisense oligonucleotide group and solvent group. Tar yellow staining and Western blotting were used to detect the neuronal damage of hippocampus and the phosphorylation of AKT and Bad (Ser136) in rat brain after ischemia-reperfusion. Results Compared with ischemia / reperfusion control group, HSP72 antisense oligodeoxynucleotide group and solvent group, heat shock treatment reduced the damage of hippocampal neurons and the phosphorylation of AKT and Bad (Ser136) in brain tissues increased (P <0.05). Conclusion HSP72 may protect hippocampal neurons by increasing the phosphorylation of AKT and Bad (Ser136) in brain tissue.