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首页> 外文期刊>Cells >Protective Effects and Target Network Analysis of Ginsenoside Rg1 in Cerebral Ischemia and Reperfusion Injury: A Comprehensive Overview of Experimental Studies
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Protective Effects and Target Network Analysis of Ginsenoside Rg1 in Cerebral Ischemia and Reperfusion Injury: A Comprehensive Overview of Experimental Studies

机译：人参皂苷Rg1对脑缺血再灌注损伤的保护作用和靶标网络分析：实验研究综述

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摘要

Cerebral ischemia-reperfusion is a complicated pathological process. The injury and cascade reactions caused by cerebral ischemia and reperfusion are characterized by high mortality, high recurrence, and high disability. However, only a limited number of antithrombotic drugs, such as recombinant tissue plasminogen activator (r-TPA), aspirin, and heparin, are currently available for ischemic stroke, and its safety concerns is inevitable which associated with reperfusion injury and hemorrhage. Therefore, it is necessary to further explore and examine some potential neuroprotective agents with treatment for cerebral ischemia and reperfusion injury to reduce safety concerns caused by antithrombotic drugs in ischemic stroke. Ginseng Rg1 (G-Rg1) is a saponin composed of natural active ingredients and derived from the roots or stems of Panax notoginseng and ginseng in traditional Chinese medicine. Its pharmacological effects exert remarkable neurotrophic and neuroprotective effects in the central nervous system. To explore and summarize the protective effects and mechanisms of ginsenoside Rg1 against cerebral ischemia and reperfusion injury, we conducted this review, in which we searched the PubMed database to obtain and organize studies concerning the pharmacological effects and mechanisms of ginsenoside Rg1 against cerebral ischemia and reperfusion injury. This study provides a valuable reference and clues for the development of new agents to combat ischemic stroke. Our summarized review and analysis show that the pharmacological effects of and mechanisms underlying ginsenoside Rg1 activity against cerebral ischemia and reperfusion injury mainly involve 4 sets of mechanisms: anti-oxidant activity and associated apoptosis via the Akt, Nrf2/HO-1, PPARγ/HO-1, extracellular regulated protein kinases (ERK), p38, and c-Jun N-terminal kinase (JNK) pathways (or mitochondrial apoptosis pathway) and the caspase-3/ROCK1/MLC pathway; anti-inflammatory and immune stimulatory-related activities that involve apoptosis or necrosis via MAPK pathways (the JNK1/2 + ERK1/2 and PPARγ/HO-1 pathways), endoplasmic reticulum stress (ERS), high mobility group protein1 (HMGB1)-induced TLR2/4/9 and receptor for advanced glycation end products (RAGE) pathways, and the activation of NF-κB; neurological cell cycle, proliferation, differentiation, and regeneration via the MAPK pathways (JNK1/2 + ERK1/2, PI3K-Akt/mTOR, PKB/Akt and HIF-1α/VEGF pathways); and energy metabolism and the regulation of cellular ATP levels, the blood-brain barrier and other effects via N-methyl-D-aspartic acid (NMDA) receptors, ERS, and AMP/AMPK-GLUT pathways. Collectively, these mechanisms result in significant neuroprotective effects against cerebral ischemic injury. These findings will be valuable in that they should further promote the development of candidate drugs and provide more information to support the application of previous findings in stroke clinical trials.
机译：脑缺血-再灌注是一个复杂的病理过程。由脑缺血和再灌注引起的损伤和级联反应的特征是高死亡率，高复发性和高残疾性。但是，目前只有有限数量的抗血栓药物，例如重组组织纤溶酶原激活剂（r-TPA），阿司匹林和肝素可用于缺血性中风，其安全性不可避免，与再灌注损伤和出血有关。因此，有必要进一步探索和研究一些潜在的神经保护剂，以治疗脑缺血和再灌注损伤，以减少缺血性卒中中抗栓药物引起的安全性问题。人参Rg1（G-Rg1）是由天然活性成分组成的皂苷，其来源于中药三七和人参的根或茎。它的药理作用在中枢神经系统中具有显着的神经营养和神经保护作用。为了探讨和总结人参皂苷Rg1对脑缺血再灌注损伤的保护作用及其机制，我们进行了综述，在PubMed数据库中搜索人参皂苷Rg1对脑缺血和再灌注的药理作用及其机理的研究。受伤。该研究为开发抗缺血性中风的新药物提供了有价值的参考和线索。我们总结的综述和分析表明，人参皂苷Rg1活性对脑缺血和再灌注损伤的药理作用和潜在机制主要涉及4组机制：抗氧化剂活性和通过Akt，Nrf2 / HO-1，PPARγ/ HO引起的相关凋亡-1，细胞外调节蛋白激酶（ERK），p38和c-Jun N末端激酶（JNK）途径（或线粒体凋亡途径）和caspase-3 / ROCK1 / MLC途径;抗炎和免疫刺激相关活动，涉及通过MAPK途径（JNK1 / 2 + ERK1 / 2和PPARγ/ HO-1途径），内质网应激（ERS），高迁移率族蛋白1（HMGB1）的凋亡或坏死诱导TLR2 / 4/9和受体的晚期糖基化终产物（RAGE）途径，并激活NF-κB;通过MAPK途径（JNK1 / 2 + ERK1 / 2，PI3K-Akt / mTOR，PKB / Akt和HIF-1α/ VEGF途径）的神经细胞周期，增殖，分化和再生; N-甲基-D-天门冬氨酸（NMDA）受体，ERS和AMP / AMPK-GLUT途径对能量代谢和细胞ATP水平，血脑屏障及其他作用的调节。这些机制共同导致对脑缺血性损伤的明显神经保护作用。这些发现将是有价值的，因为它们应进一步促进候选药物的开发，并提供更多信息以支持先前发现在中风临床试验中的应用。

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