目的 采用大鼠大腦中動(dòng)脈栓塞/再灌注（MCAO/R）模型考察注射用丹參多酚酸（SAFI）對(duì)腦缺血再灌注大鼠核因子E2相關(guān)因子2（Nrf2）/Kelch樣ECH相關(guān)蛋白（Keap1）/血紅素氧合酶-1（HO-1）信號(hào)通路的影響。方法 線栓法構(gòu)建大鼠MCAO/R模型，于術(shù)后24 h進(jìn)行神經(jīng)功能評(píng)分，將造模成功的大鼠隨機(jī)分為模型組、丁苯酞（5 mL·kg^-1）組和SAFI低、中、高劑量（5.76、11.51、23.02 mg·kg^-1）組，尾iv給藥，連續(xù)14 d?？疾旖o藥后各組大鼠神經(jīng)功能缺損評(píng)分；ELISA法檢測(cè)血清超氧化物歧化酶（SOD）、丙二醛（MDA）、腦源性神經(jīng)營(yíng)養(yǎng)因子（BDNF）水平；TTC染色法檢測(cè)腦梗死體積；HE染色觀察腦組織病理變化；Western blotting法檢測(cè)Nrf2、Keap1、HO-1蛋白表達(dá)。結(jié)果 與模型組比較，SAFI中、高劑量組和丁苯酞組大鼠的神經(jīng)功能缺損評(píng)分顯著降低（P＜0.05、0.01） ；SAFI各劑量組和丁苯酞組腦梗死體積顯著減少（P＜0.01、0.001），血清BDNF、SOD水平均顯著升高（P＜0.05、0.01、0.001），MDA水平顯著降低（P＜0.05、0.01），腦組織病理變化明顯減輕，水腫減輕； SAFI高、中劑量組及丁苯酞組Keap1、Nrf2、HO-1蛋白表達(dá)顯著升高（P＜0.05、0.01、0.001），SAFI低劑量組Keap1、HO-1蛋白表達(dá)顯著升高（P＜0.01、0.001）。結(jié)論 SAFI可以減輕大鼠腦缺血再灌注損傷，可能是通過促進(jìn)Nrf2/Keap1/HO-1信號(hào)通路，抑制氧化損傷實(shí)現(xiàn)的。

Objective To investigate the effect of Salvianolic Acid for Injectionon (SAFI) on the Nrf2/Keap1/HO-1 signaling pathway in rats with cerebral ischemia-reperfusion using the rat middle cerebral artery occlusion/reperfusion (MCAO/R) model. Methods The rats were constructed with MCAO/R model using suture method, and rats with successful modeling were randomly divided into model groups, butylphthalide (5 mL·kg^-1) group, SAFI low, medium, and high dose (5.76, 11.51, and 23.02 mg·kg^-1) group, with 17 rats in each group. According to the volume of 5 mL·kg^-1, the rats in each group were injected into the tail vein for 14 d. After administration, the severity of neurological impairment in each group was scored. The contents of superoxide dismutase (SOD), malondialdehyde (MDA) and brain-derived neurotrophic factor (BDNF) in ischemic cerebral tissue were detected by ELISA. TTC staining was used to detect the cerebral infarct size. HE staining was used to observe the pathological changes of brain tissue. The expression of Nrf2/Keap1/HO-1 related pathway protein was detected by Western blotting. Results Compared with the model group, the neurological deficit scores of rats in the SAFI medium, high-dose, and butylphthalide groups were significantly reduced (P＜0.05, 0.01). The cerebral infarction volume was significantly reduced (P＜0.01, 0.001) in each dose group of SAFI and the butylphthalide group, while serum BDNF and SOD levels were significantly increased (P＜0.05, 0.01, 0.001), MDA levels were significantly reduced (P＜0.05, 0.01), pathological changes in brain tissue were significantly reduced, and edema was alleviated. The expression of Keap1, Nrf2, and HO-1 proteins was significantly increased in the high and medium dose SAFI groups and the butylphthalide group (P＜0.05, 0.01, 0.001), while the expression of Keap1 and HO-1 proteins was significantly increased in the low dose SAFI group (P＜0.01, 0.001). Conclusion SAFI can alleviate cerebral ischemia-reperfusion injury in rats. Its mechanism of action may be related to promote the Nrf2/Keap1/HO-1 signaling pathway and inhibiting oxidative damage.

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