Department of Histology and Cell Biology, Faculty of Medicine, Assiut University, Assiut, Egypt.
Department of Medical Physiology, Faculty of Medicine, Assiut University, Assiut, Egypt.
Mol Biol Rep. 2019 Dec;46(6):5841-5858. doi: 10.1007/s11033-019-05018-9. Epub 2019 Aug 8.
Parkinson's disease (PD) is a chronic neurodegenerative disease. Unfortunately, the effectiveness of anti-Parkinson treatments gradually diminishes owing to the progressive degeneration of the dopaminergic terminals. The research described here investigated the effect of adipose-derived mesenchymal stem cells (AD-MSC) versus that of an anti-Parkinson drug in a rat model of Parkinsonism. Forty adult rats were divided into four equal groups, each group receiving a different treatment: vehicle, rotenone, rotenone + AD-MSC, or rotenone + carbidopa/levodopa. Behavioral tests were carried out before and at the end of the treatment and specimens harvested from the midbrain were processed for light and electron microscopy. Genetic expression of glial fibrillary acidic protein (GFAP) and Nestin mRNA was assessed. Expression of the Lamin-B1 and Vimentin genes was measured, along with plasma levels of Angiopoietin-2 and dopamine. Treatment with rotenone induced pronounced motor deficits, as well as neuronal and glial alterations. The AD-MSC group showed improvements in motor function in the live animals and in the microscopic picture presented by their tissues. The fold change of both genes (GFAP and Nestin) decreased significantly in the AD-MSC and carbidopa/levodopa groups compared to the group with Parkinson's disease. Plasma levels of Angiopoietin-2 and dopamine were significantly increased after treatment (P < 0.001) compared to levels in the rats with Parkinson's disease. AD-MSC reduced neuronal degeneration more efficiently than did the anti-Parkinson drug in a rat model of Parkinsonism.
帕金森病(PD)是一种慢性神经退行性疾病。不幸的是,由于多巴胺能末梢的进行性退化,抗帕金森病治疗的效果逐渐减弱。这里描述的研究调查了脂肪间充质干细胞(AD-MSC)与抗帕金森病药物在帕金森病大鼠模型中的效果。40 只成年大鼠被分为四组,每组接受不同的治疗:载体、鱼藤酮、鱼藤酮+AD-MSC 或鱼藤酮+卡比多巴/左旋多巴。在治疗前和治疗结束时进行行为测试,并对中脑标本进行光镜和电镜处理。评估神经胶质纤维酸性蛋白(GFAP)和巢蛋白 mRNA 的基因表达。测量 Lamin-B1 和 Vimentin 基因的表达,以及血管生成素-2 和多巴胺的血浆水平。鱼藤酮治疗引起明显的运动功能障碍,以及神经元和神经胶质改变。AD-MSC 组在活动物和组织的显微镜图片中显示运动功能得到改善。与帕金森病组相比,AD-MSC 和卡比多巴/左旋多巴组的两种基因(GFAP 和 Nestin)的倍数变化显著降低。与帕金森病大鼠相比,治疗后(P<0.001)血管生成素-2 和多巴胺的血浆水平显著升高。AD-MSC 比抗帕金森病药物更有效地减少神经元退化在帕金森病大鼠模型中。