Evidence map›Paper›PMID 28608236›Full record

ArticleNeurochemical research2017

The Neuroprotective Effect of Curcumin Against Nicotine-Induced Neurotoxicity is Mediated by CREB-BDNF Signaling Pathway.

Majid Motaghinejad, Manijeh Motevalian, Sulail Fatima, Fahimeh Faraji, Shiva Mozaffari

Abstract read
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Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
–field-weighted citation impact
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

46 citing papers in PubMed.

  1. Article
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  4. Enhancing Neuroprotection Through Exercise: The Synergistic Effects of Bioactive Plant Compounds Via the CREB-BDNF Signaling Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
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  7. Antioxidant Properties ofCombinatorial chemistry & high throughput screening · 2025
    Article
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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

5 authors.

Majid MotaghinejadRazi Drug Research Center and Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Hemmat High Way, Beside Milad Tower, P. O. Box 14496-14525, Tehran, Iran. Dr.motaghinejad6@gmail.com.
Manijeh MotevalianRazi Drug Research Center and Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Hemmat High Way, Beside Milad Tower, P. O. Box 14496-14525, Tehran, Iran.
Sulail FatimaRazi Drug Research Center and Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Hemmat High Way, Beside Milad Tower, P. O. Box 14496-14525, Tehran, Iran.
Fahimeh FarajiRazi Drug Research Center and Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Hemmat High Way, Beside Milad Tower, P. O. Box 14496-14525, Tehran, Iran.
Shiva MozaffariPolymer Engineering, Islamic Azad University of Tehran, Science and Research Branch, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nicotine abuse adversely affects brain and causes apoptotic neurodegeneration. Curcumin- a bright yellow chemical compound found in turmeric is associated with neuroprotective properties. The current study was designed to evaluate the role of CREB-BDNF signaling in mediating the neuroprotective effects of curcumin against nicotine-induced apoptosis, oxidative stress and inflammation in rats. Sixty adult male rats were divided randomly into six groups. Group 1 received 0.7 ml/rat normal saline, group 2 received 6 mg/kg nicotine. Groups 3, 4, 5 and 6 were treated concurrently with nicotine (6 mg/kg) and curcumin (10, 20, 40 and 60 mg/kg i.p. respectively) for 21 days. Open Field Test (OFT) was used to evaluate the motor activity. Hippocampal oxidative, anti-oxidant, inflammatory and apoptotic factors were evaluated. Furthermore, phosphorylated brain cyclic adenosine monophosphate (cAMP) response element binding protein (P-CREB) and brain derived neurotrophic factor (BDNF) levels were studied at gene and protein levels. We found that nicotine disturbed the motor activity in OFT and simultaneous treatment with curcumin (40 and 60 mg/kg) reduced the nicotine-induced motor activity disturbances. In addition, nicotine treatment increased lipid peroxidation and the levels of GSH, IL-1β, TNF-α and Bax, while reducing Bcl-2, P-CREB and BDNF levels in the hippocampus. Nicotine also reduced the activity of superoxide dismutase, glutathione peroxidase and glutathione reductase in hippocampus. In contrast, various doses of curcumin attenuated nicotine-induced apoptosis, oxidative stress and inflammation; while elevating P-CREB and BDNF levels. Thus, curcumin via activation of P-CREB/BDNF signaling pathway, confers neuroprotection against nicotine-induced inflammation, apoptosis and oxidative stress.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCyclic AMP Response Element-Binding ProteinHippocampusMaleNeuroprotectionNeuroprotective AgentsNeurotoxicity SyndromesNicotineOxidative StressRatsSignal TransductionBrain-Derived Neurotrophic FactorCyclic AMP Response Element-Binding ProteinNeuroprotective AgentsNicotineBDNFCREBCurcuminNeurodegenerationNicotine

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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.