Evidence map›Paper›PMID 35812142›Full record

ArticleSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society2022

Empagliflozin attenuates neurodegeneration through antioxidant, anti-inflammatory, and modulation of α-synuclein and Parkin levels in rotenone-induced Parkinson's disease in rats.

Sanaa Ahmed, Mahmoud M El-Sayed, Mohamed A Kandeil, Marwa M Khalaf

Open access · hybridAbstract read
In one paragraph

Article in Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

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  14. Empagliflozin Mitigates PTZ-Induced Seizures in Rats: Modulating Npas4 and CREB-BDNF Signaling Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
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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

4 authors at 2 institutions in 1 country.

Sanaa AhmedPharmacology Department, Faculty of Medicine, Sohag University, Sohag 82524, Egypt.
Mahmoud M El-SayedPharmacology & Toxicology Department, Faculty of Pharmacy, Beni-Suef University, Beni-Suef 62514, Egypt.
Mohamed A KandeilBiochemistry Department, Faculty of Veterinary Medicine, Beni-Suef University, Beni-Suef 62514, Egypt.
Marwa M KhalafPharmacology & Toxicology Department, Faculty of Pharmacy, Beni-Suef University, Beni-Suef 62514, Egypt.
Beni-Suef University · EGSohag University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sodium-glucose co-transporter 2 (SGLT 2) inhibitors are a relatively new antidiabetic drug with antioxidant and anti-inflammatory properties. Therefore, this study aimed to investigate whether SGLT 2 inhibitors have a neuroprotective effect in PD. Twenty-four Wistar rats were randomized into four groups. The first one (control group) received dimethyl sulfoxide (DMSO) as a vehicle (0.2 mL/48 hr, S.C). The second group (positive control) received rotenone (ROT) (2.5 mg/kg/48 hr, S.C) for 20 successive days, whereas the third and fourth groups received empagliflozin (EMP) (1 and 2 mg/kg/day, orally), respectively. The two groups received rotenone (2.5 mg/kg/48 hr S.C) concomitantly with EMP for another 20 days on the fifth day. By the end of the experimental period, behavioral examinations were done. Subsequently, rats were sacrificed, blood samples and brain tissues were collected for analysis. ROT significantly elevated oxidative stress and proinflammatory markers as well as α-synuclein. However, dopamine (DP), antioxidants, tyrosine hydroxylase (TH), and Parkin were significantly decreased. Groups of (EMP + ROT) significantly maintained oxidative stress and inflammatory markers elevation, maintained α-synuclein and Parkin levels, and elevated TH activity and dopamine level. In both low and high doses, EMP produced a neuroprotective effect against the PD rat model, with the high dose inducing a more significant effect.

Indexed as

CP, CeruloplasminDMSO, Dimethyl sulphoxideDOPAC, Dihydrophenyl acetic acidDOPAL, DihydroxyphenylacetaldehydeDP, DopamineEMP, EmpagliflozinGABA, γ-Aminobutyric acidGSH, Reduced glutathioneIL-1β, Interlukine 1βMAO, Monoamine oxidaseMDA, MalondialdehydeNeurodegenerationNeuroprotectionNO, Nitric oxideParkinsonismPD, Parkinson’s diseaseROS, Reactive oxygen speciesRotenoneROT, RotenoneSGLT-2 inhibitorsSGLT 2, Sodium glucose co-transporter 2SOD, Superoxide dismutaseTH, Tyrosine hydroxylaseTNF-α, Tumor necrosis factor–αα–syn, Alpha-synuclienα-synuclein

Identifiers

PMID35812142
PMCPMC9257853
OpenAlexW4283388764

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

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.