PUBLICATION

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

Authors
Dongjie, S., Rajendran, R.S., Xia, Q., She, G., Tu, P., Zhang, Y., Liu, K.
ID
ZDB-PUB-220215-5
Date
2022
Source
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie   148: 112706 (Journal)
Registered Authors
Keywords
Antioxidant, Dopamine, MPTP, Parkinson disease, Traditional Chinese medicine
MeSH Terms
  • 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/pharmacology
  • 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/therapeutic use
  • Animals
  • Disease Models, Animal
  • Dopaminergic Neurons
  • MPTP Poisoning*/drug therapy
  • Medicine, Chinese Traditional
  • Mice
  • Mice, Inbred C57BL
  • Neuroprotective Agents*/therapeutic use
  • Parkinson Disease*/drug therapy
  • Parkinson Disease*/metabolism
  • Zebrafish
PubMed
35152046 Full text @ Biomed. Pharmacother.
Abstract
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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