PhysiologyDepartment, National Organization for Drug Control and Research (NODCAR), Giza, Egypt.
Histology Department, National Organization for Drug Control and Research (NODCAR), Giza, Egypt.
Biomed Pharmacother. 2020 Oct;130:110473. doi: 10.1016/j.biopha.2020.110473. Epub 2020 Jul 21.
Despite the fact that levodopa has proven its effectiveness in treating the symptoms of Parkinson's disease (PD), increasing concerns have emerged about its possible long-term toxic effects on dopamine (DA) neurons. The study investigated the possible ameliorative effect of virgin coconut oil against l-dopa- induced neurotoxicity in adult rats. A total number of 40 rats were divided into four groups. Briefly, the first served as control, the second was orally administered virgin coconut oil (1.42 mL/kg), the third group was administered a single daily dose of l-dopa/carbidopa (100/10 mg/kg/day, p.o) and the fourth group pre-treated with virgin coconut oil then administered a single daily dose of l-dopa/carbidopa. The different treatments were extended for 30 days. l-dopa treated group exhibited aggressive behavior and behavioral abnormalities in open field test compared to control group. In addition, l-dopa treatment caused significant increase in the levels of striatal dopamine and norepinephrine and their metabolites with concomitant decrease of serotonin and its metabolite. Moreover, l-dopa treatment increased histamine and GABA levels. In addition, l-dopa treatment induced oxidative stress and energy crisis. The histological and immunohistochemical studies showed that l-dopa caused a remarkable neurodegeneration and increased glial fibrillary acidic protein (GFAP) immunoexpression in the striatal area. Virgin coconut oil co-treatment significantly minimized the harmful effects of l-dopa. In conclusion, the present study revealed that virgin coconut oil provided a notable protection against l-dopa's untoward effects.
尽管左旋多巴已被证明在治疗帕金森病(PD)的症状方面有效,但人们越来越关注其对多巴胺(DA)神经元可能产生的长期毒性作用。本研究调查了初榨椰子油对成年大鼠左旋多巴诱导的神经毒性的可能改善作用。总共 40 只大鼠被分为四组。简而言之,第一组作为对照组,第二组口服初榨椰子油(1.42 毫升/千克),第三组每天给予一次左旋多巴/卡比多巴(100/10 毫克/千克/天,口服),第四组用初榨椰子油预处理,然后每天给予一次左旋多巴/卡比多巴。不同的治疗方案持续了 30 天。与对照组相比,左旋多巴治疗组在旷场试验中表现出攻击性行为和行为异常。此外,左旋多巴治疗导致纹状体多巴胺和去甲肾上腺素及其代谢物水平显著升高,同时导致 5-羟色胺及其代谢物水平降低。此外,左旋多巴治疗增加了组胺和 GABA 水平。此外,左旋多巴治疗诱导氧化应激和能量危机。组织学和免疫组织化学研究表明,左旋多巴导致纹状体区域显著的神经退行性变和胶质纤维酸性蛋白(GFAP)免疫表达增加。初榨椰子油共同处理显著减轻了左旋多巴的有害影响。总之,本研究表明,初榨椰子油对左旋多巴的不良作用提供了显著的保护作用。