Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brasil.
J Psychopharmacol. 2011 Feb;25(2):274-80. doi: 10.1177/0269881109106925. Epub 2009 Nov 25.
Cannabidiol (CBD), a Cannabis sativa constituent, may present a pharmacological profile similar to mood stabilizing drugs, in addition to anti-oxidative and neuroprotective properties. The present study aims to directly investigate the effects of CBD in an animal model of mania induced by D-amphetamine (D-AMPH). In the first model (reversal treatment), rats received saline or D-AMPH (2 mg/kg) once daily intraperitoneal (i.p.) for 14 days, and from the 8th to the 14th day, they were treated with saline or CBD (15, 30 or 60 mg/kg) i.p. twice a day. In the second model (prevention treatment), rats were pretreated with saline or CBD (15, 30, or 60 mg/kg) regime i.p. twice a day, and from the 8th to the 14th day, they also received saline or D-AMPH i.p. once daily. In the hippocampus CBD (15 mg/kg) reversed the d-AMPH-induced damage and increased (30 mg/kg) brain-derived neurotrophic factor (BDNF) expression. In the second experiment, CBD (30 or 60 mg/kg) prevented the D-AMPH-induced formation of carbonyl group in the prefrontal cortex. In the hippocampus and striatum the D-AMPH-induced damage was prevented by CBD (15, 30 or 60 mg/kg). At both treatments CBD did not present any effect against d-AMPH-induced hyperactivity. In conclusion, we could not observe effects on locomotion, but CBD protect against d-AMPH-induced oxidative protein damage and increased BDNF levels in the reversal model and these effects vary depending on the brain regions evaluated and doses of CBD administered.
大麻二酚（CBD）是大麻的一种成分，可能具有类似于稳定情绪的药物的药理学特征，此外还有抗氧化和神经保护作用。本研究旨在通过安非他命（D-AMPH）诱导的躁狂动物模型直接研究 CBD 的作用。在第一个模型（逆转治疗）中，大鼠每天腹腔内（i.p.）接受生理盐水或 D-AMPH（2mg/kg）一次，共 14 天，从第 8 天到第 14 天，它们接受生理盐水或 CBD（15、30 或 60mg/kg）i.p.每天两次。在第二个模型（预防治疗）中，大鼠每天两次接受生理盐水或 CBD（15、30 或 60mg/kg）i.p.预处理，从第 8 天到第 14 天，它们还接受 D-AMPH i.p.每天一次。在海马体中，CBD（15mg/kg）逆转了 d-AMPH 引起的损伤并增加了脑源性神经营养因子（BDNF）的表达。在第二个实验中，CBD（30 或 60mg/kg）预防了前额叶皮质中羰基的形成。在海马体和纹状体中，CBD（15、30 或 60mg/kg）预防了 D-AMPH 引起的损伤。在两种治疗中，CBD 对 d-AMPH 引起的过度活动均无作用。总之，我们没有观察到运动活动的影响，但 CBD 在逆转模型中可防止 d-AMPH 引起的氧化蛋白损伤并增加 BDNF 水平，这些作用取决于所评估的大脑区域和给予的 CBD 剂量。
