Song Fu-Xia, Wang Li, Liu Hong, Wang Ying-Li, Zou Yong
Department of Neurology, Yantai Yuhuangding Hospital, Yantai, Shandong 264000, P.R. China.
Department of Integrated Traditional and Western Medicine, Yantai Yuhuangding Hospital, Yantai, Shandong 264000, P.R. China.
Exp Ther Med. 2017 Jun;13(6):2771-2774. doi: 10.3892/etm.2017.4322. Epub 2017 Apr 10.
The present study was designed to test the hypothesis that butylphthalide protects the brain of Alzheimer's disease (AD) model rats by inhibiting apoptosis. Ninety Sprague-Dawley rats were randomly divided into drug, control and blank groups of 30 rats in each. The rats in the drug and control groups were treated to induce AD. Then, the rats in the drug group were administered with butylphthalide daily, the rats in the AD control group were given normal saline, and the rats in the healthy group were fed routinely. All rats were sacrificed after 30 days; the brain tissues were used for testing for apoptosis by the terminal deoxynucleotidyl-transferase-mediated dUTP nick end labelling (TUNEL) staining method, for determining mitogen-activated protein kinase (MAPK), ERK and P21 protein by western blot analysis, and their cognate mRNA levels by RT-PCR. The results of the TUNEL staining indicated that apoptosis of the brain tissues of rats in the drug group was significantly less than that in the control group and blank group. The protein expression levels of MAPK in the drug group were significantly lower than that in the control group, but higher than that in the normal healthy group (P<0.05). The mRNA expression levels of MAPK in the drug group were significantly lower than those in the control group, but higher than those in the normal healthy group (P<0.05). Based on these results, butylphthalide showed a protective apoptosis-inhibition effect on the brain tissues of the AD rats and this seems to be a consequence of its inhibition of the expressions of MAPK mRNA and MAPK protein in the brain of the rat.
丁苯酞通过抑制细胞凋亡来保护阿尔茨海默病（AD）模型大鼠的大脑。将90只Sprague-Dawley大鼠随机分为药物组、对照组和空白组，每组30只。对药物组和对照组的大鼠进行处理以诱导AD。然后，药物组大鼠每日给予丁苯酞，AD对照组大鼠给予生理盐水，健康组大鼠正常饲养。30天后处死所有大鼠；取脑组织采用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）染色法检测细胞凋亡，采用蛋白质免疫印迹法检测丝裂原活化蛋白激酶（MAPK）、细胞外调节蛋白激酶（ERK）和P21蛋白，并采用逆转录聚合酶链反应（RT-PCR）检测其相应mRNA水平。TUNEL染色结果表明，药物组大鼠脑组织的细胞凋亡明显少于对照组和空白组。药物组MAPK的蛋白表达水平明显低于对照组，但高于正常健康组（P<0.05）。药物组MAPK的mRNA表达水平明显低于对照组，但高于正常健康组（P<0.05）。基于这些结果，丁苯酞对AD大鼠脑组织具有保护性抗凋亡作用，这似乎是其抑制大鼠脑中MAPK mRNA和MAPK蛋白表达的结果。
