Research Institute for Korean Medicine, Yangsan Campus of Pusan National University, Yangsan-si, Republic of Korea.
College of Medicine, Dongguk University, Ilsandong-gu, Republic of Korea.
Pharm Biol. 2021 Dec;59(1):662-671. doi: 10.1080/13880209.2021.1928241.
Traditionally, the root of Nakai (Umbelliferae), has long been used to treat ischaemic diseases and is considered safe in humans.
To investigate the neuroprotective effects of a methanol extract of root (AGmex) on the middle cerebral artery occlusion (MCAO)-induced brain injury in mice, and the underlying mechanisms.
Two hours of transient MCAO (tMCAO) was induced in C57BL/6 mice (MCAO control group and AGmex groups), AGmex was administered to the AGmex group at 300-3,000 mg/kg bw at 1, 1, and 24 h before tMCAO or at 1000 mg/kg bw at 1 h before and after tMCAO. Infarction volumes, tissue staining, and western blotting were used to investigate the mechanism underlying the neuroprotective effects of AGmex.
The median effective dose (ED) could not be measured because the AGmex treatment did not reduce the infarction volume caused by 2 h of tMCAO to within 50%; however, pre-treatment with AGmex twice at 1,000 mg/kg bw before tMCAO significantly reduced the infarction volumes. The proteins related to cell growth, differentiation, and death were upregulated by this treatment, and the major recovery mechanisms appeared to involve the attenuation of the mitochondrial function of Bcl-2/Bax and activation of the PI3K/AKT/mTOR and MAPK signalling pathways in ischaemic neurons.
This study provides evidence supporting the use of root against ischaemic stroke and suggests a novel developmental starting point for the treatment of ischaemic stroke.
传统上，当归根（伞形科）长期以来一直被用于治疗缺血性疾病，并且被认为对人类是安全的。
研究当归甲醇提取物（AGmex）对小鼠大脑中动脉闭塞（MCAO）诱导的脑损伤的神经保护作用及其机制。
在 C57BL/6 小鼠中诱导 2 小时的短暂性 MCAO（tMCAO）（MCAO 对照组和 AGmex 组），AGmex 在 tMCAO 前 1、1 和 24 小时以 300-3000mg/kg bw，或 tMCAO 前 1 小时和后 1 小时以 1000mg/kg bw 给予 AGmex 组。采用梗死体积、组织染色和 Western blot 检测 AGmex 神经保护作用的机制。
由于 AGmex 治疗未能将 2 小时 tMCAO 引起的梗死体积减少到 50%以内，因此无法测量中位有效剂量（ED）；然而，在 tMCAO 前两次以 1000mg/kg bw 预先给予 AGmex 可显著减少梗死体积。这种治疗上调了与细胞生长、分化和死亡相关的蛋白质，主要的恢复机制似乎涉及 Bcl-2/Bax 的线粒体功能减弱和 PI3K/AKT/mTOR 和 MAPK 信号通路的激活。
本研究为当归根治疗缺血性中风提供了证据，并为缺血性中风的治疗提供了一个新的发展起点。
