A Systematic Review of the Biological Effects of Cordycepin.

A Systematic Review of the Biological Effects of Cordycepin.
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DOI:
10.3390/molecules26195886
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发表时间:
2021-09-28
期刊:
Molecules (Basel, Switzerland)
影响因子:
--
通讯作者:
de Moor CH
de Moor CH
中科院分区:
其他
文献类型:
--
作者:
Radhi M;Ashraf S;Lawrence S;Tranholm AA;Wellham PAD;Hafeez A;Khamis AS;Thomas R;McWilliams D;de Moor CH

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我们对虫草素对细胞存活和增殖、炎症、信号转导和动物模型的影响进行了系统的文献综述。截止到2021年2月1日,共检索到1204篇有关虫草素的文献。在应用排除标准后,仍有791篇论文。这些都被阅读了,并提取了关于选定对象的数据。我们找到了192篇关于虫草素对细胞存活和增殖的影响的文章,并计算出虫草素对细胞迁移(26篇)和细胞炎症(53篇)的半数抑制浓度(IC50)为135µM。对76篇关于信号转导的文章的评估表明,PI3K/mTOR/AKT和ERK信号转导和AMPK激活持续减少。相反,虫草素对p38和Jun激酶的影响是不同的,对细胞周期停滞的影响也是不同的(53篇文献),表明这些是细胞特异性反应。150项动物研究表明,纯化虫草素具有多种潜在的治疗作用,包括抑制肿瘤生长(37篇)、抑制疼痛和炎症(9篇)、保护脑功能(11篇)、改善呼吸和心脏状况(8篇和19篇)和改善代谢紊乱(8篇)。几乎所有这些数据都与虫草素通过激活AMPK、抑制PI3K/mTOR/AKT和抑制炎症反应而介导其治疗作用相一致。我们得出结论,虫草素作为药物开发的先导具有很好的潜力,特别是在治疗与年龄相关的疾病方面。此外,我们还讨论了虫草素的作用机制、毒性和生物分布等方面的剩余问题。
We conducted a systematic review of the literature on the effects of cordycepin on cell survival and proliferation, inflammation, signal transduction and animal models. A total of 1204 publications on cordycepin were found by the cut-off date of 1 February 2021. After application of the exclusion criteria, 791 papers remained. These were read and data on the chosen subjects were extracted. We found 192 papers on the effects of cordycepin on cell survival and proliferation and calculated a median inhibitory concentration (IC50) of 135 µM. Cordycepin consistently repressed cell migration (26 papers) and cellular inflammation (53 papers). Evaluation of 76 papers on signal transduction indicated consistently reduced PI3K/mTOR/AKT and ERK signalling and activation of AMPK. In contrast, the effects of cordycepin on the p38 and Jun kinases were variable, as were the effects on cell cycle arrest (53 papers), suggesting these are cell-specific responses. The examination of 150 animal studies indicated that purified cordycepin has many potential therapeutic effects, including the reduction of tumour growth (37 papers), repression of pain and inflammation (9 papers), protecting brain function (11 papers), improvement of respiratory and cardiac conditions (8 and 19 papers) and amelioration of metabolic disorders (8 papers). Nearly all these data are consistent with cordycepin mediating its therapeutic effects through activating AMPK, inhibiting PI3K/mTOR/AKT and repressing the inflammatory response. We conclude that cordycepin has excellent potential as a lead for drug development, especially for age-related diseases. In addition, we discuss the remaining issues around the mechanism of action, toxicity and biodistribution of cordycepin.
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