Evidence map›Paper›PMID 25197628›Full record

ArticleJournal of diabetes and metabolic disorders2014

Protective effect of magnesium on renal function in STZ-induced diabetic rats.

Mohammad Reza Parvizi, Mohsen Parviz, Seyed Mohammad Tavangar, Nepton Soltani, Mehri Kadkhodaee, Behjat Seifi, Yaser Azizi, Mansoor Keshavarz

Open access · hybridAbstract read
In one paragraph

Article in Journal of diabetes and metabolic disorders, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

21 citing papers in PubMed, 51 citations in OpenAlex.

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  15. The Role of Mitochondrial DNA (mtDNA) in the Development of Diabetic Retinopathy (DR): A Systematic Review.Medical hypothesis, discovery & innovation ophthalmology journal · 2017
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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 2 institutions in 1 country.

Mohammad Reza ParviziDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mohsen ParvizDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Seyed Mohammad TavangarDepartment of Pathology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Nepton SoltaniDepartment of Physiology, School of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
Mehri KadkhodaeeDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Behjat SeifiDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Yaser AziziDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mansoor KeshavarzDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Tehran University of Medical Sciences · IRHormozgan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic nephropathy is a serious complication of T1D (type one diabetes mellitus). Persistent hyperglycemia and subsequent hypomagnesemia is believed to develop kidney damage by activation of oxidative stress. We conducted this study to investigate the renoprotective effect of magnesium sulfate (MgSO4) on renal histopathology and oxidative stress in diabetic rats.

methodsThe study included 70 male rats. The animals were divided into seven groups: control (CRL), control receiving MgSO4 (CRL + Mg1 & CRL + Mg8), diabetic (DM1 & DM8) and diabetic receiving MgSO4 (DM + Mg1 & DM + Mg8). Rats were given 20 mg/kg (i.p) Streptozocin (STZ) for 5 consecutive days in (MLD) multiple low doses to induce T1D. At day 10 treatment groups were received MgSO4 (10 g/l) in drinking water, for 1 or 8 weeks. The blood glucose, BUN and creatinine levels were measured. Renal tissue levels of malondialdehyde (MDA) were measured by thiobarbituric acid (TBA) method to evaluate the oxidative stress. Renal histopathology was done using H & E staining method.

resultsTreatment with MgSO4 significantly decreased the blood glucose in DM + Mg1 and DM + Mg8 groups as compared with DM1 and DM8. Magnesium treatment also decreased serum BUN and tissue level of MDA significantly in both short and long term treatment. The body weight loss and kidney weight to body weight ratio was improved by MgSO4. Histological results showed there were no differences between DM and DM + Mg groups.

conclusionOur findings showed that diabetic nephropathy is associated with high blood glucose level and oxidative stress (significant increase in MDA level). The renal dysfunction and oxidative stress can be improved by magnesium sulfate administration. It is suggested that protection against development of diabetic nephropathy by MgSO4 treatment involves changes in the blood glucose and oxidative stress.

Indexed as

Diabetes mellitus type 1Diabetic nephropathyOxidative stressStreptozocin

Identifiers

PMID25197628
PMCPMC4156611
OpenAlexW2138944374

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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.