Swaroop R Sai, Pradhan Sai Sanwid, Darshan V M Datta, Phalguna Kanikaram Sai, Sivaramakrishnan Venketesh
Disease Biology Lab, Department of Biosciences, Sri Sathya Sai Institute of Higher Learning, Prasanthi Nilayam, Anantapur, Andhra Pradesh 515134 India.
3 Biotech. 2022 Dec;12(12):333. doi: 10.1007/s13205-022-03401-1. Epub 2022 Oct 31.
Amyotrophic lateral Sclerosis is an incurable, progressive neurodegenerative motor neuron disease. The disease is characterized by protein aggregates. The symptoms include weakness, denervation of muscles, atrophy and progressive paralysis of bulbar and respiratory muscles and dysphagia. Various secondary metabolites are evaluated for their ability to improve symptoms in ALS. Ginseng has been traditionally used for treating several neurodegenerative diseases. Several studies using model systems have shown a potential role of Ginseng catechins and Ginsenosides in clearing protein aggregation associated with ALS. We focus on Network pharmacology approach to understand the effect of Ginseng catechins or ginsenosides on protein aggregation associated with ALS. A catechin/ginsenoside-protein interaction network was generated and the pathways obtained were compared with those obtained from transcriptomic datasets of ALS from GEO database. Knock out of MAPK14, AKT and GSK from Catechin and BACE 1 from ginsenoside modulated pathways inhibited protein aggregation. Catechins and ginsenosides have potential as therapeutic agents in the management of ALS.
The online version contains supplementary material available at 10.1007/s13205-022-03401-1.
肌萎缩侧索硬化症是一种无法治愈的进行性神经退行性运动神经元疾病。该疾病以蛋白质聚集体为特征。症状包括虚弱、肌肉失神经支配、萎缩以及延髓和呼吸肌的进行性麻痹和吞咽困难。人们评估了各种次生代谢产物改善肌萎缩侧索硬化症症状的能力。人参传统上一直用于治疗多种神经退行性疾病。几项使用模型系统的研究表明,人参儿茶素和人参皂苷在清除与肌萎缩侧索硬化症相关的蛋白质聚集中具有潜在作用。我们专注于网络药理学方法来了解人参儿茶素或人参皂苷对与肌萎缩侧索硬化症相关的蛋白质聚集的影响。生成了儿茶素/人参皂苷-蛋白质相互作用网络,并将获得的途径与从基因表达综合数据库(GEO数据库)中肌萎缩侧索硬化症的转录组数据集获得的途径进行了比较。从儿茶素调节的途径中敲除丝裂原活化蛋白激酶14(MAPK14)、蛋白激酶B(AKT)和糖原合成酶激酶(GSK)以及从人参皂苷调节的途径中敲除β-分泌酶1(BACE 1)可抑制蛋白质聚集。儿茶素和人参皂苷在肌萎缩侧索硬化症的治疗中具有作为治疗剂的潜力。
在线版本包含可在10.1007/s13205-022-03401-1获取的补充材料。