Shi Yi-Hua, Li Yan, Wang Yong, Xu Zhen, Fu Huan, Zheng Guo-Qing
Department of Neurology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
Front Pharmacol. 2020 Mar 31;11:285. doi: 10.3389/fphar.2020.00285. eCollection 2020.
Ischemic stroke is the most common type of stroke, while pharmacological therapy options are limited. Ginsenosides are the major bioactive compounds in Ginseng and have been found to have various pharmacological effects in the nervous system. In the present study, we sought to evaluate the effects of Ginsenoside-Rb1 (G-Rb1), an important ingredient of ginsenosides, and the probable neuroprotective mechanisms in experimental ischemic strokes.
Studies of G-Rb1 on ischemic stroke animal models were identified from 7 databases. No clinical trials were included in the analysis. The primary outcome measures were neurological function scores, infarct volume, evans blue content and/or brain water content (BWC). The second outcome measures were the possible neuroprotective mechanisms. All the data were analyzed by Rev Man 5.3.
Pooled preclinical data showed that compared with the controls, G-Rb1 could improve neurological function (Zea Longa (n = 367, P < 0.01); mNSS (n = 70, P < 0.01); Water maze test (n = 48, P < 0.01); Bederson (n = 16, P < 0.01)), infarct area (TTC (n = 211, P < 0.01); HE (n = 26, P < 0.01)), as well as blood-brain barrier function (BWC (n = 64, P < 0.01); Evans blue content (n=26, P < 0.05)). It also can increase BDNF (n = 26, P < 0.01), Gap-43 (n = 16, P < 0.01), SOD (n = 30, P < 0.01), GSH (n = 16, P < 0.01), Nissl-positive cells (n = 12, P < 0.01), Nestin-positive cells (n = 10, P < 0.05), and reduce Caspase-3 (n = 36, P < 0.01), IL-1 (n = 32, P < 0.01), TNF-α (n = 72, P < 0.01), MDA (n = 18, P < 0.01), NO (n = 44, P < 0.01), NOX (n = 32, P < 0.05), ROS (n = 6, P < 0.05), NF-κB (P < 0.05) and TUNEL-positive cells (n = 52, P < 0.01).
Available findings demonstrated the preclinical evidence that G-Rb1 has a potential neuroprotective effect, largely through attenuating brain water content, promoting the bioactivities of neurogenesis, anti-apoptosis, anti-oxidative, anti-inflammatory, energy supplement and cerebral circulation.
缺血性中风是最常见的中风类型，而药物治疗选择有限。人参皂苷是人参中的主要生物活性化合物，已发现其在神经系统中具有多种药理作用。在本研究中，我们试图评估人参皂苷的重要成分人参皂苷-Rb1（G-Rb1）的作用以及实验性缺血性中风中可能的神经保护机制。
从7个数据库中确定了关于G-Rb1对缺血性中风动物模型的研究。分析中未纳入临床试验。主要结局指标为神经功能评分、梗死体积、伊文思蓝含量和/或脑含水量（BWC）。次要结局指标为可能的神经保护机制。所有数据均采用Rev Man 5.3进行分析。
汇总的临床前数据显示，与对照组相比，G-Rb1可改善神经功能（Zea Longa评分（n = 367，P < 0.01）；mNSS评分（n = 70，P < 0.01）；水迷宫试验（n = 48，P < 0.01）；Bederson评分（n = 16，P < 0.01））、梗死面积（TTC染色（n = 211，P < 0.01）；HE染色（n = 26，P < 0.01））以及血脑屏障功能（BWC（n = 64，P < 0.01）；伊文思蓝含量（n = 26，P < 0.05））。它还可增加脑源性神经营养因子（BDNF）（n = 26，P < 0.01）、生长相关蛋白43（Gap-43）（n = 16，P < 0.01）、超氧化物歧化酶（SOD）（n = 30，P < 0.01）、谷胱甘肽（GSH）（n = 16，P < 0.01）、尼氏染色阳性细胞（n = 12，P < 0.01）、巢蛋白阳性细胞（n = 10，P <
