大麻二酚的分子靶点神经障碍。
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陈Ibeas波黑C、T、南都AV Bazelot M,达拉斯,惠利BJ
大麻二酚的分子靶点神经障碍。
神经病治疗。2015年10月,12 (4):699 - 730。doi: 10.1007 / s13311 - 015 - 0377 - 3。
- PubMed ID
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26264914 (在PubMed]
- 文摘
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历史悠久的轶事药用大麻和有限许可药用。直到最近,涉嫌从轶事报告和临床疗效的使用许可大麻素药物是最有可能由四氢大麻醇由于:1)这大麻素中最大量出现在这些准备工作;和b)比例:效力之间的关系四氢大麻酚和其它植物大麻类来自大麻。然而,最近有相当大的兴趣在植物大麻素的治疗潜力,大麻二酚(CBD),在神经系统疾病,但目前的证据表明,CBD不直接与神经系统除了体外supraphysiological浓度。因此,作为CBD的进一步证据的有利影响神经系统疾病出现,仍迫切需要建立的分子靶点发挥其治疗效果。在这里,我们进行了一次系统的现存文献的搜索原始文章描述CBD的分必威国际app子药理学。我们批判性地评价结果的有效性提出的分子靶点。此后,我们考虑是否CBD的分子靶点识别相关神经系统疾病治疗的潜力。确定的分子靶点包括众多经典的离子通道,受体,转运蛋白和酶。一些CBD的影响在这些目标在体外实验中只体现在高浓度时,体内可能很难实现,尤其是鉴于CBD的相对贫穷的生物利用度。 Moreover, several targets were asserted through experimental designs that demonstrate only correlation with a given target rather than a causal proof. When the molecular targets of CBD that were physiologically plausible were considered for their potential for exploitation in neurological therapeutics, the results were variable. In some cases, the targets identified had little or no established link to the diseases considered. In others, molecular targets of CBD were entirely consistent with those already actively exploited in relevant, clinically used, neurological treatments. Finally, CBD was found to act upon a number of targets that are linked to neurological therapeutics but that its actions were not consistent withmodulation of such targets that would derive a therapeutically beneficial outcome. Overall, we find that while >65 discrete molecular targets have been reported in the literature for CBD, a relatively limited number represent plausible targets for the drug's action in neurological disorders when judged by the criteria we set. We conclude that CBD is very unlikely to exert effects in neurological diseases through modulation of the endocannabinoid system. Moreover, a number of other molecular targets of CBD reported in the literature are unlikely to be of relevance owing to effects only being observed at supraphysiological concentrations. Of interest and after excluding unlikely and implausible targets, the remaining molecular targets of CBD with plausible evidence for involvement in therapeutic effects in neurological disorders (e.g., voltage-dependent anion channel 1, G protein-coupled receptor 55, CaV3.x, etc.) are associated with either the regulation of, or responses to changes in, intracellular calcium levels. While no causal proof yet exists for CBD's effects at these targets, they represent the most probable for such investigations and should be prioritized in further studies of CBD's therapeutic mechanism of action.
DrugBank数据引用了这篇文章
- 药物
- 药物靶点
- 药物酶
- 药物转运蛋白
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药物 转运体 类 生物 药理作用 行动 大麻二酚 磷酸腺苷盒式sub-family 2 G的成员 蛋白质 人类 未知的抑制剂细节 大麻二酚 Equilibrative核苷转运体1 蛋白质 人类 未知的抑制剂细节 大麻二酚 耐多药resistance-associated蛋白1 蛋白质 人类 未知的抑制剂细节 医疗大麻 磷酸腺苷盒式sub-family 2 G的成员 蛋白质 人类 未知的抑制剂细节 医疗大麻 Equilibrative核苷转运体1 蛋白质 人类 未知的抑制剂细节 医疗大麻 耐多药resistance-associated蛋白1 蛋白质 人类 未知的抑制剂细节 Nabiximols 磷酸腺苷盒式sub-family 2 G的成员 蛋白质 人类 未知的抑制剂细节 Nabiximols Equilibrative核苷转运体1 蛋白质 人类 未知的抑制剂细节 Nabiximols 耐多药resistance-associated蛋白1 蛋白质 人类 未知的抑制剂细节