Cannabinoids and brain injury: therapeutic implications
Cannabinoids and brain injury: therapeutic implications
复制标题
DOI：
10.1016/s1471-4914(02)02276-1
复制
发表时间：
2002-02-01
影响因子：
13.6
通讯作者：
Shohami, E
中科院分区：
文献类型：
--
作者：
Mechoulam, R;Panikashvili, D;Shohami, E
体外和体内数据表明，内源性大麻素anandamide和2-arachidonoyl甘油，以及一些植物和合成大麻素，具有脑损伤后的神经保护作用。大麻素受体激动剂抑制神经元能突触传递并减少肿瘤坏死因子-a和活性氧中间体的产生，这些是引起神经元损伤的因素。内源性大麻素anandamide和2-arachidonoyl甘油的形成在脑损伤后强烈增强，并且有证据表明这些化合物减少了继发性损伤。一些不与大麻素受体结合的植物和合成大麻素也被证明具有神经保护作用，可能是通过它们对兴奋性谷氨酸系统的直接作用和/或作为抗氧化剂。
Mounting in vitro and in vivo data suggest that the endocannabinoids anandamide and 2-arachidonoyl glycerol, as well as some plant and synthetic cannabinoids, have neuroprotective effects following brain injury. Cannabinoid receptor agonists inhibit glutamatergic synaptic transmission and reduce the production of tumour necrosis factor-a and reactive oxygen intermediates, which are factors in causing neuronal damage. The formation of the endocannabinoids anandamide and 2-arachidonoyl glycerol is strongly enhanced after brain injury, and there is evidence that these compounds reduce the secondary damage incurred. Some plant and synthetic cannabinoids, which do not bind to the cannabinoid receptors, have also been shown to be neuroprotective, possibly through their direct effect on the excitatory glutamate system and/or as antioxidants.