Evidence map›Paper›PMID 27506528›Full record

ArticleInflammopharmacology2016

Anti-inflammatory effect of AMPK signaling pathway in rat model of diabetic neuropathy.

Amin Hasanvand, Hossein Amini-Khoei, Mohammad-Reza Hadian, Alireza Abdollahi, Seyed Mohammad Tavangar, Ahmad Reza Dehpour, Elika Semiei, Shahram Ejtemaei Mehr

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Article in Inflammopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 74 citations in OpenAlex.

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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 3 institutions in 1 country.

Amin HasanvandDepartment of Pharmacology, School of Medicine, International Campus, Tehran University of Medical Sciences (IC-TUMS), Tehran, Iran.
Hossein Amini-KhoeiDepartment of Pharmacology, School of Medicine, Kashan University of Medical Sciences, Kashan, Iran.
Mohammad-Reza HadianDepartment of Physical Therapy, Rehabilitation Faculty, Tehran University of Medical Sciences, Tehran, Iran.
Alireza AbdollahiDepartment of Pathology, Imam Khomini Complex Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Seyed Mohammad TavangarDepartment of Pathology, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Ahmad Reza DehpourDepartment of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Elika SemieiDepartment of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Shahram Ejtemaei MehrDepartment of Pharmacology, School of Medicine, International Campus, Tehran University of Medical Sciences (IC-TUMS), Tehran, Iran. ejtemam@gmail.com.
Tehran University of Medical Sciences · IRImam Khomeini Hospital · IRKashan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic neuropathy (DN) is characterized as Hyperglycemia activates thdisturbed nerve conduction and progressive chronic pain. Inflammatory mediators, particularly cytokines, have a determinant role in the pathogenesis of neuropathic pain. The activity of adenosine monophosphate protein kinase (AMPK), an energy charge sensor with neuroprotective properties, is decreased in diabetes. It has been reported that activation of AMPK reduces the systemic inflammation through inhibition of cytokines. In this study, we aimed to investigate the probable protective effects of AMPK on DN in a rat of diabetes. DN was induced by injection of streptozotocin (65 mg/kg, i.p.). Motor nerve conduction velocities (MNCV) of the sciatic nerve, as an electrophysiological marker for peripheral nerve damage, were measured. Plasma levels of IL-6, TNF-α, CRP were assessed as relevant markers for inflammatory response. Also, the expression of phosphorylated AMPK (p-AMPK) and non-phosphorylated (non-p-AMPK) was evaluated by western blotting in the dorsal root ganglia. Histopathological assessment was performed to determine the extent of nerve damage in sciatic nerve. Our findings showed that activation of AMPK by metformin (300 mg/kg) significantly increased the MNCV and reduced the levels of inflammatory cytokines. In addition, we showed that administration of metformin increased the expression of p-AMPK as well as decline in the level of non p-AMPK. Our results demonstrated that co-administration of dorsomorphin with metformin reversed the beneficial effects of metformin. In conclusion, the results of this study demonstrated that the activation of AMPK signaling pathway in diabetic neuropathy might be associated with the anti-inflammatory response.

Indexed as

Disease Models, AnimalAMP-Activated Protein KinasesAnimalsDiabetes Mellitus, ExperimentalDiabetic NeuropathiesHypoglycemic AgentsInflammation MediatorsMaleMetforminRandom AllocationRatsRats, WistarSignal TransductionAMP-Activated Protein KinasesHypoglycemic AgentsInflammation MediatorsMetforminAMPKCytokinesDiabetic neuropathyInflammatory responseMNCVRat

Identifiers

PMID27506528
OpenAlexW2512659802

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.