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研究丹酚酸A(SAA)减轻大鼠脑缺血再灌注损伤的机制。SD大鼠随机分组,线栓法制备大鼠大脑中动脉闭塞/再灌注(MCAO/R)模型,缺血1.5 h,再灌注24 h,对神经行为学缺损程度评分,TTC法测定大鼠脑梗死体积,Western blot测定脑组织胞核、胞浆Nrf2和全细胞HO-1蛋白含量。PC12细胞系制备缺糖缺氧复糖复氧(OGD/R)模型,缺糖缺氧6 h,复糖复氧24 h,MTT法检测细胞存活率,免疫荧光法测定Nrf2和HO-1表达,应用Nrf2 si RNA对SAA的作用机制进行研究。MCAO/R导致脑组织出现病理性损伤,OGD/R导致PC12细胞存活率显著降低。SAA(10和20 mg·kg~(-1))可使脑组织神经细胞损伤明显减轻,并且SAA(0.5和5μmol·L~(-1))能增加PC12细胞存活率。同时SAA能够促进脑组织及PC12胞核和胞浆中Nrf2蛋白表达,核转位率升高,HO-1蛋白表达增强。SAA具有抗脑缺血再灌注损伤的作用,其机制可能与激活Nrf2/HO-1信号途径,促进Nrf2合成和核转位,从而促进下游抗氧化蛋白HO-1的表达有关。
To study the mechanism of Salvianolic acid A (SAA) attenuating cerebral ischemia-reperfusion injury in rats. SD rats were randomly divided into the middle cerebral artery occlusion / reperfusion (MCAO / R) model. The rats were subjected to cerebral ischemia / reperfusion (MCAO / R) for 1.5 h and reperfused for 24 h. The neurobehavioral deficits were assessed. Infarct volume and Western blot were used to determine the content of Nrf2 and whole cell HO-1 in the nucleus and cytoplasm. The model of hypoglycemic hypoxia and hypoxia and reoxygenation (OGD / R) was established in PC12 cell line. The hypoxia and hypoxia for 6 h, reoxygenation for 24 h, MTT assay and Nrf2 and HO-1 expression were detected by immunofluorescence , The application of Nrf2 si RNA on SAA mechanism of action. MCAO / R resulted in pathological damage of brain tissue, OGD / R resulted in significantly lower survival rate of PC12 cells. SAA (10 and 20 mg · kg -1) significantly reduced the damage of nerve cells in brain tissue, and SAA (0.5 and 5 μmol·L -1) increased the survival rate of PC12 cells. At the same time, SAA could promote the expression of Nrf2 protein in the nucleus and cytoplasm of brain and PC12, and the nuclear translocation rate and HO-1 protein expression increased. SAA can prevent cerebral ischemia-reperfusion injury and its mechanism may be related to activating Nrf2 / HO-1 signaling pathway, promoting Nrf2 synthesis and nuclear translocation, and promoting the expression of downstream antioxidant protein HO-1.