Department of Pharmacology, Faculty of Pharmacy, The University of Lahore, Lahore, Pakistan.
Department of Pharmacology, Faculty of Pharmacy, The University of Lahore, Lahore, Pakistan/Faculty of Pharmacy, University of Central Punjab, Lahore, Pakistan.
Pak J Pharm Sci. 2020 Mar;33(2(Supplementary)):755-763.
The study was designed to investigate the neuro-protection of lauric acid (LA) on haloperidol (HPD) induced Parkinson's disease (PkD) rat model. Rats were divided into group A (normal), group B (diseased, by HPD 1mg/kg i.p. for 14 days), group C (standard treatment, levodopa 30 mg/kg), group D (vehicle coconut oil 1ml/kg), group E (LA 0.66mg/kg) and group F (LA 1.32mg/kg) for 35 days after induction of PkD. The study displayed a state of oxidative stress in the striatum of rat model of PkD as shown from the increased MDA, NO levels and the decreased superoxide dismutase levels. HPD caused an increase in tumor necrosis factor-α level, NF-κB, IL-8 mRNA expression and suppress IL-4 expression. Neuro-protection with LA attenuated the oxidative stress and changes in pro-inflammatory cytokines induced due to PkD induction. The LA treatment also showed improvement in the histo-pathology of the rats' brain. LA also improved behavioral performances, food intake, weight gain as compared to animal of diseased group and prevented decline in motor activities (assessed Rotarod, and Beam walking test). LA showed significant neuro-protection against oxidative stress, inflammatory cytokines and behavioral changes in HPD induced rat model of PkD.
这项研究旨在探讨月桂酸（LA）对氟哌啶醇（HPD）诱导的帕金森病（PkD）大鼠模型的神经保护作用。大鼠被分为 A 组（正常）、B 组（疾病组，腹腔注射 HPD1mg/kg 14 天）、C 组（标准治疗组，左旋多巴 30mg/kg）、D 组（载体椰子油 1ml/kg）、E 组（LA0.66mg/kg）和 F 组（LA1.32mg/kg），在诱导 PkD 后 35 天进行治疗。研究显示，PkD 大鼠模型纹状体存在氧化应激状态，表现为 MDA、NO 水平升高，超氧化物歧化酶水平降低。HPD 导致肿瘤坏死因子-α水平、NF-κB、IL-8mRNA 表达增加，IL-4 表达抑制。LA 的神经保护作用可减轻 PkD 诱导的氧化应激和促炎细胞因子的变化。LA 治疗还改善了大鼠大脑的组织病理学。与疾病组动物相比，LA 还改善了行为表现、食物摄入和体重增加，防止了运动活动（旋转棒和横梁行走测试）的下降。LA 对 HPD 诱导的 PkD 大鼠模型的氧化应激、炎症细胞因子和行为变化具有显著的神经保护作用。
