Evidence map›Paper›PMID 32351675›Full record

ArticleOxidative medicine and cellular longevity2020

TBHQ Attenuates Neurotoxicity Induced by Methamphetamine in the VTA through the Nrf2/HO-1 and PI3K/AKT Signaling Pathways.

Xianyi Meng, Chenghong Zhang, Yu Guo, Ying Han, Chunyang Wang, Haiying Chu, Li Kong, Haiying Ma

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 46 citations in OpenAlex.

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  19. Frontiers in pharmacology · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Xianyi MengDepartment of Histology and Embryology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, China.ORCID https://orcid.org/0000-0002-6988-0961
Chenghong ZhangDepartment of Histology and Embryology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, China.ORCID https://orcid.org/0000-0001-8826-5895
Yu GuoDepartment of Histology and Embryology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, China.
Ying HanDepartment of Histology and Embryology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, China.
Chunyang WangDepartment of Histology and Embryology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, China.
Haiying ChuDepartment of Histology and Embryology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, China.ORCID https://orcid.org/0000-0002-5591-9968
Li KongDepartment of Histology and Embryology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, China.
Haiying MaDepartment of Histology and Embryology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, China.ORCID https://orcid.org/0000-0002-1314-7816
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AnimalsAntioxidantsHydroquinonesMaleMethamphetamineNeurotoxicity SyndromesNF-E2-Related Factor 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRats, WistarSignal Transduction2-tert-butylhydroquinoneAntioxidantsHydroquinonesMethamphetamineNF-E2-Related Factor 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID32351675
PMCPMC7174937
OpenAlexW3016010536

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.