1-Trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo) Induces the Apoptosis of Dopaminergic Neurons via Oxidative Stress and Neuroinflammation
Joint Authors
Yang, Yihang
Pang, Bo
Liu, Zihao
Li, Jie
Zhang, Zhen
Zhang, Rui
Hou, Xianzeng
Guo, Hua
Chi, Lingyi
Pang, Qi
Xin, Tao
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-12, 12 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-03-07
Country of Publication
Egypt
No. of Pages
12
Main Subjects
Abstract EN
Several in vitro studies have revealed the neurotoxicity of 1-trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo).
However, the underlying mechanism has not been completely elucidated, particularly in vivo.
This study was designed to study the neurotoxicity of TaClo in vivo by stereotactically injecting TaClo into the striatum of Wistar rats.
After the TaClo injections, rats were subjected to an open field test, and their distance travelled and tracks showed decreasing trends over time.
The results of liquid chromatography-mass spectrometry analysis showed that the motor dysfunction of the TaClo-treated rats was accompanied by reduced dopamine levels in the striatum.
Based on the diffusion tensor imaging data, the apparent diffusion coefficient of the nigrostriatal pathway was significantly increased, and subsequent histological staining revealed the demyelination of nigrostriatal fibres after the TaClo treatment.
TaClo induced a loss of tyrosine hydroxylase-positive cells in the substantia nigra compacta.
Regarding the underlying mechanism, TaClo caused oxidative stress in the nigrostriatal system by increasing the production of reactive oxygen species and reducing the mitochondria membrane potential.
Meanwhile, the elevated expression of Iba-1, TNF-α, IL-6, Cox-2, and iNOS indicated microglial activation and a strong innate immune response in the nigrostriatal system.
In addition, activated caspase-3 levels were increased.
Thus, both mitochondrial impairments and the innate immune response are involved in TaClo-induced neurotoxicity.
American Psychological Association (APA)
Yang, Yihang& Pang, Bo& Liu, Zihao& Li, Jie& Zhang, Zhen& Zhang, Rui…[et al.]. 2019. 1-Trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo) Induces the Apoptosis of Dopaminergic Neurons via Oxidative Stress and Neuroinflammation. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-12.
https://search.emarefa.net/detail/BIM-1202084
Modern Language Association (MLA)
Yang, Yihang…[et al.]. 1-Trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo) Induces the Apoptosis of Dopaminergic Neurons via Oxidative Stress and Neuroinflammation. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-12.
https://search.emarefa.net/detail/BIM-1202084
American Medical Association (AMA)
Yang, Yihang& Pang, Bo& Liu, Zihao& Li, Jie& Zhang, Zhen& Zhang, Rui…[et al.]. 1-Trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo) Induces the Apoptosis of Dopaminergic Neurons via Oxidative Stress and Neuroinflammation. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-12.
https://search.emarefa.net/detail/BIM-1202084
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1202084