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Neuroprotective effects of Tongtian oral liquid, a Traditional Chinese Medicine in the Parkinson's disease-induced zebrafish model

MPTP公司 多巴胺能 神经保护 药理学 斑马鱼 氧化应激 多巴胺 神经毒性 帕金森病 超氧化物歧化酶 化学 生物 神经科学 医学 内科学 生物化学 毒性 疾病 基因
作者
Dongjie Shan,R. Samuel Rajendran,Qing Xia,Gaimei She,Pengfei Tu,Yun Zhang,Kechun Liu
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier BV]
卷期号:148: 112706-112706 被引量:22
标识
DOI:10.1016/j.biopha.2022.112706
摘要

Traditional Chinese medicine (TCM) is used in the treatment of Parkinson's disease (PD) worldwide. Tongtian Oral Liquid (TTKFY) is one such patented TCM, and a poly-herbal formulation, composed of 11 herbal constituents, which possess neuroprotective, antioxidant, pain-relieving properties. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP), a neurotoxicant is used to induce PD in animal models. The present study was aimed to evaluate the neuroprotective effects of TTKFY, on dopaminergic neuron development, antioxidant activities, and gene expression involved in the dopaminergic pathway in the MPTP-treated zebrafish model. Zebrafish larvae were treated with MPTP (70 μM) to induce PD and then by different concentrations (0.5, 1, 2, 4 ml/L) of TTKFY. Transgenic zebrafish Vmat: GFP at 5 dpf were used to observe the development of dopaminergic neurons. The activities of T-Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), malonaldehyde (MDA) and mRNA gene expression of dopamine pathway were quantified. MPTP-treated zebrafish larvae showed degeneration of dopaminergic neurons, locomotion dysfunction, diminished activities of antioxidant enzymes, MDA accumulation, and altered gene expression of dopamine pathway. In contrast, TTKFY protected dopaminergic neurons, ameliorated behavioral impairments, antioxidant activities and mRNA gene expression of dopamine pathway in a dose-dependent manner. Thus, TTKFY confers protective effects against MPTP-induced neurotoxicity and the mechanisms of protection may be related to the recovery of dopaminergic neurons by reducing oxidative stress via restoring cellular defense mechanisms and thereby highlighting its therapeutic potential to prevent the progression of PD. Further studies are necessary to elucidate the mechanism of action of TTKFY on neuroprotection in the MPTP-induced PD model.
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