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目的:观察左旋四氢巴马汀(L-THP)对局灶性脑缺血再灌注损伤的保护作用及对神经元凋亡蛋白P53、HSP70表达的影响,探讨L-THP的神经保护作用及机制。方法:采用改良Longa法建立局灶性脑缺血再灌注模型,11分法对大鼠进行神经行为症状评分,比色法测定大鼠血清乳酸脱氢酶(LDH)活力,HE染色观察大鼠脑组织神经元病理形态学变化,免疫组织化学染色法分别检测缺血侧海马CA1区P53、HSP70阳性细胞表达。结果:L-THP能够明显改善局灶性脑缺血再灌注损伤大鼠神经行为症状以及脑组织形态结构,降低血清LDH活力,并且能够降低大鼠海马CA1区P53蛋白的阳性表达,在再灌注早期增强HSP70的阳性表达。结论:L-THP对局灶性脑缺血再灌注损伤具有保护作用,其作用机制可能与抑制凋亡蛋白P53的表达,增强HSP70的表达有关。
AIM: To observe the protective effect of L-THP on focal cerebral ischemia-reperfusion injury and its effect on the expression of neuronal apoptosis proteins P53 and HSP70 and the neuroprotective effect of L-THP mechanism. Methods: The model of focal cerebral ischemia-reperfusion was established by the modified Longa method. The neurobehavioral symptoms of rats were evaluated by the method of eleven minutes. The activity of lactate dehydrogenase (LDH) in serum was measured by colorimetric method. Pathological changes of neurons in brain tissue were detected by immunohistochemical staining for the expression of P53 and HSP70 positive cells in hippocampal CA1 area. Results: L-THP could significantly improve neurobehavioral symptoms, morphological structure of brain tissue and serum LDH activity in rats with focal cerebral ischemia / reperfusion injury and reduce the positive expression of P53 protein in hippocampal CA1 region. Early enhanced HSP70 positive expression. CONCLUSION: L-THP has a protective effect on focal cerebral ischemia-reperfusion injury. Its mechanism may be related to inhibiting the expression of P53 and enhancing the expression of HSP70.