左旋四氢巴马汀对局灶性脑缺血再灌注大鼠凋亡蛋白P53、HSP70表达的影响

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.

Effects of L-tetrahydropalmatine(L-THP)on the Expression of Apoptosis Protein P53 and HSP70 after Focal Cerebral Ischemia Reperfusion Injury in Rats

Objective： To explore the neuroprotective mechanism of L-THP by observation of the protective effects of L-THP and expression of nerve cell apoptosis protein P53 and HSP70 after focal cerebral isehemia reperfusion injury in Rats. Method： Modified Longa method were employed to establish focal cerebral ischemia reperfusion animal models, the neurological deficits were monitored, lactate dehydrogenase （LDH） level was examined by colorimetry,the morphological change was observed by HE dyeing, and immuno- histochemical method was used to analyze the expression of P53 and HSP70 apoptosis protein positive cells. Result： L-THP could im- prove nervalsymptom and cerebral tissue, decrease the activitie of LDH and reduce the level of P53, increase the expression of HSP70 in himppocampal CA1. Conclusion： L-THP has the protective effect on focal cerebral isehemia repeffusion injure. Its mechanism may be associated with the inhibition of apoptosis protein P53 expression and increase of HSP70.