Evidence map›Paper›PMID 28258522›Full record

ArticleInflammopharmacology2017

Sitagliptin and liraglutide reversed nigrostriatal degeneration of rodent brain in rotenone-induced Parkinson's disease.

Ghada A Badawi, Mai A Abd El Fattah, Hala F Zaki, Moushira I El Sayed

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Article in Inflammopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.9field-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

64 citing papers in PubMed, 117 citations in OpenAlex.

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4 more citing papers are in PubMed but not listed here.

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.

Ghada A BadawiDepartment of Pharmacology and Toxicology, Faculty of Pharmacy and Pharmaceutical Industries, Sinai University, El-Arish, Egypt. ghadaali1986@yahoo.com.
Mai A Abd El FattahDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
Hala F ZakiDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
Moushira I El SayedDepartment of Pharmacology and Toxicology, Faculty of Pharmacy and Pharmaceutical Industries, Sinai University, El-Arish, Egypt.
Cairo University · EGSinai University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study investigated the possible relationship between pro-inflammatory cytokines and programmed nigral neuronal death in rotenone model of Parkinson's disease (PD). Sitagliptin and liraglutide efficacy to inhibit the inflammatory-apoptotic degenerative process were investigated, too. The experimental PD were induced in male albino rats by ten subcutaneously injections of rotenone (3 mg/kg/day, s.c). All treatment drugs were administered for 16 days after induction of Parkinson rat's model. Sitagliptin and liraglutide were administered in three different dose levels (10-20-30 mg/kg, p.o), (25-50-100 μg/kg, s.c), respectively. Cylindrical and catalepsy tests were used to detect the optimum dose response of each drug. Sitagliptin (30 mg/kg/day, p.o) and liraglutide (50 μg/kg, s.c.) showed statistically significant (p ≤ 0.05) effect on behavioral activity. Where both doses improved the motor performance significantly in comparison with other doses in both cylindrical and catalepsy tests. Furthermore, they reversed rotenone-induced nigral neuronal loss, associated with marked decrease of pro-inflammatory cytokines: interleukin (IL)-1β, IL-6, transforming growth factor (TGF)-β1, together with a significant increase of striatal dopamine, nigral glial cell line-derived neurotrophic factor (GDNF), and tyrosine hydroxylase positive (TH+) cells. Moreover, the pro-apoptotic environment in nigrostriatal tissues was abrogated significantly, as the pro-apoptotic protein Bax decreased along with the anti-apoptotic protein Bcl-2 increased. In conclusion, sitagliptin and liraglutide represent a promising strategy to mitigate the progression of PD by their anti-inflammatory, anti-apoptotic neurotrophic and neurogenic mechanistic activities.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinBrainDisease Models, AnimalGlial Cell Line-Derived Neurotrophic FactorInterleukin-1betaInterleukin-6LiraglutideMaleParkinson DiseaseProto-Oncogene Proteins c-bcl-2RatsRodentiaRotenoneSitagliptin Phosphatebcl-2-Associated X ProteinGlial Cell Line-Derived Neurotrophic FactorInterleukin-1betaInterleukin-6LiraglutideProto-Oncogene Proteins c-bcl-2RotenoneSitagliptin PhosphateTransforming Growth Factor beta1Tyrosine 3-MonooxygenaseApoptosisGDNFIL-1βIL-6LiraglutidePDRotenoneSitagliptinTGF-β1

Identifiers

PMID28258522
OpenAlexW2593866083

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.