Department of Clinical Pharmacology, Faculty of Medicine, Suez Canal University, 41522 Ismailia, Egypt; Central Laboratory, Center of Excellence in Molecular and Cellular Medicine (CEMCM), Faculty of Medicine, Suez Canal University, 41522 Ismailia, Egypt.
Department of Human Physiology, Faculty of Medicine, Suez Canal University, 41522 Ismailia, Egypt.
J Chem Neuroanat. 2023 Jan;127:102206. doi: 10.1016/j.jchemneu.2022.102206. Epub 2022 Dec 1.
Parkinson's disease (PD) is a neurodegenerative illness described as damage to dopaminergic neurons. There is increasing evidence that neuroinflammatory activity mediated by microglia is extensively involved in the initiation and development of PD. This study assessed the protective effect of evening primrose oil [EPO] as an anti-inflammatory mediator in rotenone-induced Parkinsonism in rats. Forty-eight adult male albino rats were distributed into four groups. Group I: control. Group II: rotenone [1.5 mg/kg/48 h] was administered subcutaneously to the rats. Groups III and IV: the rats had rotenone plus daily oral [EPO] 5 and 10 mg/kg respectively. After 24 days, motor behaviour was assessed by the open field and rotarod tests. The brain striata were isolated and tested for tumor necrosis factor (TNF)-α, interleukin 6, NF-B [nuclear factor-kappa B], and dopamine levels. The mid-brain tissues were processed for light and electron microscopy examinations, and immunohistochemical staining for tyrosine hydroxylase [TH], and microglia cells' markers: [CD68 and IBA1]. Results revealed that rotenone-treated rats had poor motor function, a significantly increased striatal level of inflammatory markers, markedly shrunken neurons, degeneration, pyknotic neuroglia, neuropil vacuolation, markedly destructed swollen mitochondria with loss of their cristae, and dilated rough endoplasmic reticulum, as well as decreased TH and increased CD68 and IBA1-positive cells. Treatment with EPO ameliorates all the neuropathological changes of rotenone in the rat brain. In conclusion, EPO enhanced the motor performance, reduced the inflammatory marker levels, restored dopamine levels, and ameliorated the neurohistopathological lesions of rats with experimental parkinsonism, suggesting its neuroprotective and anti-inflammatory effects.
帕金森病（PD）是一种神经退行性疾病，其特征是多巴胺能神经元受损。越来越多的证据表明，小胶质细胞介导的神经炎症活性广泛参与了 PD 的起始和发展。本研究评估了月见草油[EPO]作为一种抗炎介质在鱼藤酮诱导的大鼠帕金森病中的保护作用。48 只成年雄性白化大鼠分为四组。第 I 组：对照组。第 II 组：皮下给予大鼠鱼藤酮[1.5mg/kg/48h]。第 III 组和第 IV 组：大鼠分别口服鱼藤酮加每日 5 和 10mg/kg 的 EPO。24 天后，通过旷场和转棒试验评估运动行为。分离大脑纹状体并检测肿瘤坏死因子（TNF）-α、白细胞介素 6、NF-B[核因子-κB]和多巴胺水平。对中脑组织进行光镜和电镜检查，以及酪氨酸羟化酶[TH]和小胶质细胞标志物[CD68 和 IBA1]的免疫组织化学染色。结果表明，鱼藤酮处理的大鼠运动功能差，纹状体炎症标志物水平显著升高，神经元明显萎缩，变性，神经胶质固缩，神经胶质空泡形成，肿胀的线粒体明显破坏，嵴丢失，扩张的粗面内质网，以及 TH 减少和 CD68 和 IBA1 阳性细胞增加。EPO 治疗改善了大鼠大脑中鱼藤酮的所有神经病理学变化。总之，EPO 增强了运动表现，降低了炎症标志物水平，恢复了多巴胺水平，并改善了实验性帕金森病大鼠的神经组织病理学损伤，提示其具有神经保护和抗炎作用。
