Sarne Yosef, Mechoulam Raphael
Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv 69978, Israel.
Curr Drug Targets CNS Neurol Disord. 2005 Dec;4(6):677-84. doi: 10.2174/156800705774933005.
Cannabinoids, such as the delta9-tetrahydrocannabinol (THC), present in the cannabis plant, as well as anandamide and 2-arachidonoyl glycerol, produced by the mammalian body, have been shown to protect the brain from various insults and to improve several neurodegenerative diseases. The current review summarizes the evidence for cannabinoid neuroprotection in vivo, and refers to recent in vitro studies, which help elucidate possible molecular mechanisms underlying this protective effect. Some of these mechanisms involve the activation of CB1 and CB2 cannabinoid receptors, while others are not dependent on them. In some cases, protection is due to a direct effect of the cannabinoids on neuronal cells, while in others, it results from their effects on non-neuronal elements within the brain. In many experimental set-ups, cannabinoid neurotoxicity, particularly by THC, resides side by side with neuroprotection. The current review attempts to shed light on this dual activity, and to dissociate between the two contradictory effects.
大麻植物中存在的大麻素，如Δ9-四氢大麻酚（THC），以及哺乳动物体内产生的花生四烯乙醇胺和2-花生四烯酸甘油酯，已被证明可保护大脑免受各种损伤，并改善多种神经退行性疾病。本综述总结了大麻素在体内神经保护作用的证据，并提及了最近的体外研究，这些研究有助于阐明这种保护作用背后可能的分子机制。其中一些机制涉及CB1和CB2大麻素受体的激活，而其他机制则不依赖于它们。在某些情况下，保护作用是由于大麻素对神经元细胞的直接作用，而在其他情况下，则是由于它们对脑内非神经元成分的作用。在许多实验设置中，大麻素神经毒性，特别是THC引起的神经毒性，与神经保护作用并存。本综述试图阐明这种双重活性，并区分这两种相互矛盾的作用。
