The neuroprotective effect of NeuroAid on morphine-induced amnesia with respect to the expression of TFAM, PGC-1α, ΔfosB and CART genes in the hippocampus of male Wistar rats.


Journal

Gene
ISSN: 1879-0038
Titre abrégé: Gene
Pays: Netherlands
ID NLM: 7706761

Informations de publication

Date de publication:
05 Jun 2020
Historique:
received: 04 01 2020
revised: 16 02 2020
accepted: 16 03 2020
pubmed: 22 3 2020
medline: 2 6 2020
entrez: 22 3 2020
Statut: ppublish

Résumé

Morphine is a natural alkaloid which derived from the opium poppy Papaver somniferum. Many studies have reported the effect of morphine on learning, memory and gene expression. CART (cocaine-amphetamine regulated transcript)is an important neuropeptide which has a critical role in physiological processes including drug dependence and antioxidant activity. ΔfosB is a transcription factor which modulates synaptic plasticity and affects learning and memory. TFAM (the mitochondrial transcription factor A) and PGC-1α (Peroxisome proliferator-activated receptor γ coactivator-1α) are critically involved in mitochondrial biogenesis and antioxidant pathways. NeuroAid is a Chinese medicine that induces neuroprotective and anti-apoptotic effects. In this research, we aimed to investigate the effect of NeuroAid on morphine-induced amnesia with respect to the expression of TFAM, PGC-1α, ΔfosB and CART in the rat's hippocampus. In this study, Morphine sulfate (at increasing doses), Naloxone hydrochloride (2.5 mg/kg) and NeuroAid (2.5 mg/kg) were administered intraperitoneal and real-time PCR reactions were done to assess gene expression. The results showed, morphine impaired memory of step-through passive avoidance, while NeuroAid had no effect. NeuroAid attenuated (but not reversed) morphine-induced memory impairment in morphine-addicted rats. Morphine increased the expression of PGC-1α and decreased the expression of CART. However, NeuroAid increased the expression of TFAM, PGC-1α, ΔfosB and CART. NeuroAid restored the effect of morphine on the expression of CART and PGC-1α. In conclusion, morphine impaired memory of step-through passive avoidance and NeuroAid attenuated this effect. The effect of NeuroAid on morphine-induced memory impairment/gene expression may be related to its anti-apoptotic and neuroprotective effects.

Identifiants

pubmed: 32198124
pii: S0378-1119(20)30270-5
doi: 10.1016/j.gene.2020.144601
pii:
doi:

Substances chimiques

Drugs, Chinese Herbal 0
Fosb protein, rat 0
Nerve Tissue Proteins 0
Neuroaid 0
Neuroprotective Agents 0
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha 0
Ppargc1a protein, rat 0
Proto-Oncogene Proteins c-fos 0
Tfam protein, rat 0
Transcription Factors 0
cocaine- and amphetamine-regulated transcript protein 0
Morphine 76I7G6D29C

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

144601

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Nasrin Malboosi (N)

Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.

Mohammad Nasehi (M)

Cognitive and Neuroscience Research Center (CNRC), Amir-Almomenin Hospital, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. Electronic address: Nasehi@iricss.org.

Mehrdad Hashemi (M)

Department of Genetics, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.

Salar Vaseghi (S)

Cognitive and Neuroscience Research Center (CNRC), Amir-Almomenin Hospital, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran; Institute for Cognitive Science Studies (ICSS), Tehran, Iran.

Mohammad-Reza Zarrindast (MR)

Institute for Cognitive Science Studies (ICSS), Tehran, Iran; Department of Pharmacology School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Department of Neuroendocrinology, Endocrinology and Metabolism Research Institute, Tehran University of Medical Sciences, Tehran, Iran.

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Classifications MeSH