Medical Molecular Biology Laboratory, Medical College, Jinhua Polytechnic, Jinhua, Zhejiang, China (mainland).
Zhu Kezhen College, Zhejiang University, Hangzhou, Zhejiang, China (mainland).
Med Sci Monit. 2021 Jun 4;27:e931884. doi: 10.12659/MSM.931884.
BACKGROUND This study assessed the effects and underlying molecular mechanisms of ß-asarone on ischemic stroke model rats. MATERIAL AND METHODS Ischemic stroke was induced by middle cerebral artery occlusion (MCAO) in rats. Before and after modeling, cognitive function was evaluated via fear conditioning test and neurological deficit was determined via Longa and Bederson scores. Following treatment with ß-asarone or nuclear factor erythroid 2-related factor 2 (Nrf2) inhibitor for 20 consecutive days, the cerebral infarction was detected via TTC staining and Cresyl Violet staining in brain tissues. TUNEL staining and western blot analysis for apoptosis-related proteins were performed to assess the apoptosis of neurons. Nrf2-antioxidant response elements (ARE) pathway-related proteins were examined by RT-qPCR or western blot. RESULTS The cognitive and neurological function was defective in MCAO rats. The infarction volumes and the apoptosis of cortical neurons were significantly increased in brain tissues of model rats, which were ameliorated after treatment with ß-asarone. Meanwhile, the increase in pro-apoptotic proteins and decrease in anti-apoptotic proteins were found in brain tissues of model rats, which were markedly ameliorated by ß-asarone treatment. However, Nrf2 inhibitor worsened the cerebral infarction and the apoptosis of neurons. Western blot results showed that ß-asarone treatment activated the Nrf2-ARE pathway-related proteins in model rats, which was inhibited by Nrf2 inhibitor. CONCLUSIONS Our findings suggest that ß-asarone treatment ameliorated the cerebral infarction in MCAO rats, which could be related to activation of the Nrf2-ARE pathway.
本研究评估了β-细辛脑对缺血性脑卒中模型大鼠的作用及其潜在的分子机制。
通过大脑中动脉闭塞（MCAO）诱导大鼠缺血性脑卒中。在建模前后，通过恐惧条件反射试验评估认知功能，通过 Longa 和 Bederson 评分确定神经功能缺损。β-细辛脑或核因子红细胞 2 相关因子 2（Nrf2）抑制剂连续治疗 20 天后，通过 TTC 染色和脑组织中 Cresyl Violet 染色检测脑梗死。通过 TUNEL 染色和 Western blot 分析评估神经元凋亡相关蛋白，检测神经元凋亡。通过 RT-qPCR 或 Western blot 检测 Nrf2-抗氧化反应元件（ARE）通路相关蛋白。
MCAO 大鼠的认知和神经功能受损。模型大鼠脑组织梗死体积和皮质神经元凋亡明显增加，β-细辛脑治疗后有所改善。同时，模型大鼠脑组织中促凋亡蛋白增加，抗凋亡蛋白减少，β-细辛脑治疗后明显改善。然而，Nrf2 抑制剂加重了脑梗死和神经元凋亡。Western blot 结果显示，β-细辛脑治疗激活了模型大鼠的 Nrf2-ARE 通路相关蛋白，而 Nrf2 抑制剂则抑制了这一作用。
我们的研究结果表明，β-细辛脑治疗改善了 MCAO 大鼠的脑梗死，这可能与激活 Nrf2-ARE 通路有关。
