Alves Amanda de Deus Ferreira, Dias Fernanda Carolina Ribeiro, Cadena Pabyton Gonçalves, Silva-Jr Valdemiro Amaro
Department of Veterinary Medicine, Federal Rural University of Pernambuco, Brazil.
Department of Veterinary Medicine, Federal Rural University of Pernambuco, Brazil; Cellular Interactions Laboratory, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, MG, Brazil.
Neurotoxicology. 2024 Dec;105:34-44. doi: 10.1016/j.neuro.2024.08.002. Epub 2024 Aug 23.
This systematic review was carried out with the aim of evaluating the use of medicinal Cannabis for the treatment of Parkinson's disease in experimental models. Furthermore, we sought to understand the main intracellular mechanisms capable of promoting the effects of phytocannabinoids on motor disorders, neurodegeneration, neuroinflammation and oxidative stress. The experimental models were developed in mice, rats and marmosets. There was a predominance of using only males in relation to females; in three studies, the authors evaluated treatments in males and females. Drugs were used as inducers of Parkinson's disease: 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), lipopolysaccharide (LPS), and rotenone. Substances capable of promoting catalepsy in animals were also used: haloperidol, L-nitro-N-arginine (L-NOARG), WIN55,212-2, and reserpine. The inducing agent was injected stereotaxically or intraperitoneally. The most commonly used treatments were cannabidiol (CBD), Delta-9-tetrahydrocannabinol (Δ-9 THC) and Delta-9-tetrahydrocannabivarin (Δ-9 THCV), administered intraperitoneally, orally, subcutaneously and intramuscularly. The use of phytocannabinoids improved locomotor activity and involuntary movement and reduced catalepsy. There was an improvement in the evaluation of dopaminergic neurons, while in relation to dopamine content, the treatment had no effect. Inflammation, microglial/astrocyte activation and oxidative stress were reduced after treatment with phytocannabinoids, the same was observed in the results of tests for allodynia and hyperalgesia.
本系统评价旨在评估药用大麻在实验模型中治疗帕金森病的应用。此外,我们试图了解能够促进植物大麻素对运动障碍、神经退行性变、神经炎症和氧化应激产生作用的主要细胞内机制。实验模型是在小鼠、大鼠和狨猴身上建立的。与雌性相比,使用雄性的情况占主导;在三项研究中,作者评估了雄性和雌性的治疗情况。药物被用作帕金森病的诱导剂:6-羟基多巴胺(6-OHDA)、1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)、脂多糖(LPS)和鱼藤酮。还使用了能够在动物中促进僵住症的物质:氟哌啶醇、L-硝基-N-精氨酸(L-NOARG)、WIN55,212-2和利血平。诱导剂通过立体定向或腹腔内注射。最常用的治疗方法是腹腔内、口服、皮下和肌肉注射大麻二酚(CBD)、Δ-9-四氢大麻酚(Δ-9 THC)和Δ-9-四氢大麻萜酚(Δ-9 THCV)。植物大麻素的使用改善了运动活动和不自主运动,并减少了僵住症。多巴胺能神经元的评估有所改善,而对于多巴胺含量,治疗没有效果。植物大麻素治疗后炎症、小胶质细胞/星形胶质细胞活化和氧化应激减少,在异常性疼痛和痛觉过敏测试结果中也观察到了同样的情况。