Pérez-Barrón Gabriela, Avila-Acevedo José Guillermo, García-Bores Ana María, Montes Sergio, García-Jiménez Sara, León-Rivera Ismael, Rubio-Osornio Moisés, Monroy-Noyola Antonio
Laboratorio de Neuroprotección, Facultad de Farmacia, Universidad Autónoma del Estado de Morelos, Av. Universidad 1001 Col. Chamilpa, CP 62209, Cuernavaca, Morelos, México.
J Nat Med. 2015 Jan;69(1):86-93. doi: 10.1007/s11418-014-0866-4. Epub 2014 Sep 25.
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the irreversible loss of dopaminergic neurons in the nigrostriatal pathway with subsequent dopamine deficiency. Environmental causes have been proposed through molecules, such as 1-methyl-4-phenylpyridinium (MPP(+)), to induce oxidative stress. The methanolic extract of plants of the genus Buddleja has been reported to have in vitro and in vivo antioxidant properties to protect against neuronal death. In the present study, the neuroprotective effect of Buddleja cordata methanolic extract in the MPP(+) PD rat model was investigated. Animals were administered orally with 50 or 100 mg/kg of methanolic extract every 24 h for 14 days. Twenty hours later, rats were infused with an intrastriatal stereotaxic microinjection of 10 µg MPP(+) in 8 μl sterile saline solution. Six days later, the animals were treated with 1 mg/kg apomorphine to record ipsilateral rotations for 1 h. All the rats were killed by decapitation and the lesioned striatum was dissected for dopamine and lipid peroxidation quantifications. Both methanolic extract doses led to a significantly lower (P < 0.05) number of ipsilateral rotations (75-80 %). This behavioral protection was corroborated with 60 % level of dopamine preservation (P < 0.05) and 90 % decrease in the formation of lipidic fluorescent products in the striatum (P < 0.05). This study demonstrates the antioxidant and neuroprotective effect of Buddleja cordata methanolic extract in the MPP(+) PD rat model, possibly due to the involvement of phenylpropanoids.
帕金森病(PD)是一种神经退行性疾病,其特征是黑质纹状体通路中的多巴胺能神经元不可逆丧失,随后出现多巴胺缺乏。已提出环境因素可通过1-甲基-4-苯基吡啶鎓(MPP(+))等分子诱导氧化应激。据报道,醉鱼草属植物的甲醇提取物具有体外和体内抗氧化特性,可防止神经元死亡。在本研究中,研究了密蒙花甲醇提取物在MPP(+)帕金森病大鼠模型中的神经保护作用。动物每24小时口服50或100mg/kg甲醇提取物,持续14天。20小时后,通过纹状体内立体定向微量注射将10μg MPP(+)注入8μl无菌盐溶液中。六天后,用1mg/kg阿扑吗啡治疗动物,记录同侧旋转1小时。所有大鼠断头处死,解剖损伤的纹状体进行多巴胺和脂质过氧化定量分析。两种甲醇提取物剂量均导致同侧旋转次数显著降低(P<0.05)(降低75-80%)。这种行为保护与多巴胺保留水平60%(P<0.05)以及纹状体中脂质荧光产物形成减少90%(P<0.05)相关。本研究证明了密蒙花甲醇提取物在MPP(+)帕金森病大鼠模型中的抗氧化和神经保护作用,可能是由于苯丙烷类化合物的参与。