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TBHQ Attenuates Neurotoxicity Induced by Methamphetamine in the VTA through the Nrf2HO-1 and PI3KAKT Signaling Pathways
Joint Authors
Zhang, Chenghong
Meng, Xianyi
Chu, Haiying
Ma, Haiying
Guo, Yu
Han, Ying
Wang, Chunyang
Kong, Li
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-04-13
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Methamphetamine (METH) leads to nervous system toxicity.
Long-term exposure to METH results in damage to dopamine neurons in the ventral tegmental area (VTA), and depression-like behavior is a clinical symptom of this toxicity.
The current study was designed to investigate whether the antioxidant tertiary butylhydroquinone (TBHQ) can alleviate neurotoxicity through both antioxidative stress and antiapoptotic signaling pathways in the VTA.
Rats were randomly divided into a control group, a METH-treated group (METH group), and a METH+TBHQ-treated group (METH+TBHQ group).
Intraperitoneal injections of METH at a dose of 10 mg/kg were administered to the rats in the METH and METH+TBHQ groups for one week, and METH was then administered at a dose that increased by 1 mg/kg per week until the sixth week, when the daily dosage reached 15 mg/kg.
The rats in the METH+TBHQ group received 12.5 mg/kg TBHQ intragastrically.
Chronic exposure to METH resulted in increased immobility times in the forced swimming test (FST) and tail suspension test (TST) and led to depression-like behavior.
The production of reactive oxygen species (ROS) and apoptosis levels were increased in the VTA of animals in the METH-treated group.
METH downregulated Nrf2, HO-1, PI3K, and AKT, key factors of oxidative stress, and the apoptosis signaling pathway.
Moreover, METH increased the caspase-3 immunocontent.
These changes were reversed by treatment with the antioxidant TBHQ.
The results indicate that TBHQ can enhance Nrf2-induced antioxidative stress and PI3K-induced antiapoptotic effects, which can alleviate METH-induced ROS and apoptosis, and that the crosstalk between Nrf2 and PI3K/AKT is likely the key factor involved in the protective effect of TBHQ against METH-induced chronic nervous system toxicity.
American Psychological Association (APA)
Meng, Xianyi& Zhang, Chenghong& Guo, Yu& Han, Ying& Wang, Chunyang& Chu, Haiying…[et al.]. 2020. TBHQ Attenuates Neurotoxicity Induced by Methamphetamine in the VTA through the Nrf2HO-1 and PI3KAKT Signaling Pathways. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1205695
Modern Language Association (MLA)
Meng, Xianyi…[et al.]. TBHQ Attenuates Neurotoxicity Induced by Methamphetamine in the VTA through the Nrf2HO-1 and PI3KAKT Signaling Pathways. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-13.
https://search.emarefa.net/detail/BIM-1205695
American Medical Association (AMA)
Meng, Xianyi& Zhang, Chenghong& Guo, Yu& Han, Ying& Wang, Chunyang& Chu, Haiying…[et al.]. TBHQ Attenuates Neurotoxicity Induced by Methamphetamine in the VTA through the Nrf2HO-1 and PI3KAKT Signaling Pathways. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1205695
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1205695