Zhai L, Wang J, Ji Y Q, Wang T T, Liu M, Guo Y L
Department of Pharmacy, Qingdao Municipal Hospital Affiliated to Qingdao University, Qingdao 266071, China.
Zhonghua Yi Xue Za Zhi. 2018 Dec 4;98(45):3705-3710. doi: 10.3760/cma.j.issn.0376-2491.2018.45.015.
To investigate the effect and mechanisms of picroside Ⅱ on the brain tissue after cerebral ischemia reperfusion(I/R) in rats. The middle cerebral artery occlusion(MCAO) rat model was established by inserting a monofilament into middle cerebral artery. The experimental rats were treated by injecting picroside Ⅱ intraperitoneally. The modified neurological severity score (mNSS) and body weight were determined before modeling and after reperfusion of 22 h. The cerebral infarct volume was measured by TTC staining and the cerebral water content was measured in rats. At the same time, ROS content and NADPH oxidase activity were detected. The structure of neurons was observed by electron microscope and the mRNA and protein levels of Rac-1 and Nox2 were detected by RT-PCR and Western blotting. After modeling, the mNSS score was significantly increased (12.6±1.3 vs 0, <0.001), while the body weight was lost (13.3%±2.5% vs 4.9%±0.8%, <0.01). The cerebral infarct volume increased obviously (33.5%±3.4% vs 0, <0.001), brain water content increased significantly (81.5%±0.9% vs 77.7%±0.9%, <0.05) and the structure of neuron was damaged obviously. The protein and mRNA levels of Rac-1 and Nox2 were significantly increased (<0.05). After treatment with picroside Ⅱ, mNSS score decreased significantly (7.9±0.8 vs 12.6±1.3, <0.05) and the body weight increased obviously (9.3%±1.1% vs 13.3%±2.5%, <0.05). The infarct volume of brain was significantly reduced (18.2%±1.9% vs 33.5%±3.4%, <0.05), brain water content decreased obviously (79.1%±0.7% vs 81.5±0.9%, <0.05), the morphological structures of neurons was restored, and the expressions of Rac-1 and Nox2 were significantly decreased (<0.05). It is suggested that picroside Ⅱ could exert antioxidation to protect the brain tissue through inhibiting the expression of Rac-1 and Nox2.
探讨胡黄连苷Ⅱ对大鼠脑缺血再灌注（I/R）后脑组织的影响及其作用机制。采用线栓法插入大脑中动脉建立大脑中动脉闭塞（MCAO）大鼠模型。对实验大鼠进行腹腔注射胡黄连苷Ⅱ治疗。在建模前及再灌注22 h后测定改良神经功能缺损评分（mNSS）和体重。通过TTC染色测量脑梗死体积，测定大鼠脑含水量。同时，检测活性氧（ROS）含量和NADPH氧化酶活性。用电子显微镜观察神经元结构，采用RT-PCR和Western blotting检测Rac-1和Nox2的mRNA和蛋白水平。建模后，mNSS评分显著升高（12.6±1.3 vs 0，<0.001），而体重下降（13.3%±2.5% vs 4.9%±0.8%，<0.01）。脑梗死体积明显增加（33.5%±3.4% vs 0，<0.001），脑含水量显著增加（81.5%±0.9% vs 77.7%±0.9%，<0.05），神经元结构明显受损。Rac-1和Nox2的蛋白及mRNA水平显著升高（<0.05）。用胡黄连苷Ⅱ治疗后，mNSS评分显著降低（7.9±0.8 vs 12.6±1.3，<0.05），体重明显增加（9.3%±1.1% vs 13.3%±2.5%，<0.05）。脑梗死体积显著减小（18.2%±1.9% vs 33.5%±3.4%，<0.05），脑含水量明显降低（79.1%±0.7% vs 81.5±0.9%，<0.05），神经元形态结构恢复，Rac-1和Nox2的表达显著降低（<0.05）。提示胡黄连苷Ⅱ可能通过抑制Rac-1和Nox2的表达发挥抗氧化作用，保护脑组织。
