Evidence map›Paper›PMID 41611768›Full record

ArticleScientific reports2026

Mechanistic insights into the lipotropic and atheroprotective effects of rosuvastatin-loaded glycerosomes in dyslipidemic rats.

Mohamed Fouad Mansour, Rabab A Husseini, Samar Ahmed Abdo, Tarek Khamis, Haiam A Mohammed, Amira Ebrahim Alsemeh, Marwa Tharwat Abdelfattah, Mahran Mohamed Abd El-Emam

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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.

Mohamed Fouad MansourDepartment of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, 44519, Egypt. mafouad@zu.edu.eg.
Rabab A HusseiniDepartment of Pharmaceutics, Faculty of Pharmacy, Zagazig University, Zagazig, 44519, Egypt.
Samar Ahmed AbdoDepartment of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, 44519, Egypt.
Tarek KhamisDepartment of Pharmacology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, 44519, Egypt.
Haiam A MohammedDepartment of Physiology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, 44519, Egypt.
Amira Ebrahim AlsemehDepartment of Anatomy and Embryology, Faculty of Medicine, Zagazig University, Zagazig, 44519, Egypt.
Marwa Tharwat AbdelfattahDepartment of Anatomy and Embryology, Faculty of Medicine, Zagazig University, Zagazig, 44519, Egypt.
Mahran Mohamed Abd El-EmamDepartment of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, 44519, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dyslipidemia is a major risk factor for the development of NAFLD, atherosclerosis and cardiovascular diseases. Rosuvastatin (ROS) is a lipid-lowering drug that protects against the development of NAFLD and atherosclerosis. However, the mechanism of this protection remains obscure. Therefore, the current study aims to explore the mechanism by which ROS-loaded glycerosomes (ROS-GLY) protect against NAFLD and atherosclerosis. Hence, for this purpose, hepatic lncRNA-H19/miR-130a/PPAR-γ and aortic PPAR-γ/LXRα/ABCA1 signaling pathways were assessed. In addition, these target pathways were predicted using molecular docking analysis. Thirty-five male Sprague Dawley rats were separated into control, dyslipidemic (poloxamer 407 (P 407)), P 407+ROS-GLY, P 407+NC, and P 407+ROS-GLY+NC groups. ROS-GLY improved lipid profile, hepatic MDA, SOD, catalase and total antioxidant capacity (TAC) in compared to P 407 group. In the dyslipidemic group, ROS-GLY downregulated hepatic lncRNA-H19 expression which leads to an upregulate of the miR-130a level and subsequent reduction of the PPAR-γ level. Consequently, the hepatic expression level of lipogenic genes such as, ACC-1, FASN and SCD-1 was significantly downregulated in the ROS-GLY group than the dyslipidemic one. Aortic PPAR-γ/LXRα/ABCA1 signaling pathway was significantly upregulated in the ROS-GLY group compared to the dyslipidemic group. Furthermore, ROS-GLY modulated IL-6 and IL-10 immunoprotein expression in hepatic and aortic tissues. Interestingly, ROS showed a substantial binding affinity with PPAR-γ, LXR-α, and FASN, according to a molecular docking study. The current study indicated that ROS-GLY protected against the progression of NAFLD and atherosclerosis in dyslipidemic rats via modulation of lipid profile, oxidative stress, pro-/anti-inflammatory cytokines, hepatic lncRNA-H19/miR-130a/PPAR-γ, and aortic PPAR-γ/LXRα/ABCA1 signaling pathways.

Indexed as

AtherosclerosisDyslipidemiasRosuvastatin CalciumAnimalsATP Binding Cassette Transporter 1LiverLiver X ReceptorsMaleMicroRNAsMolecular Docking SimulationNon-alcoholic Fatty Liver DiseaseOxidative StressPPAR gammaRatsRats, Sprague-DawleySignal TransductionAbca1 protein, ratATP Binding Cassette Transporter 1Liver X ReceptorsMicroRNAsNr1h3 protein, ratPPAR gammaPPAR gamma, ratRosuvastatin CalciumAtherosclerosisDyslipidemiaLncRNA-H19/miR-130a/PPARγ pathwayNAFLDPPAR-γ/LXRα/ABCA1 pathwayRosuvastatin-glycerosomes

Identifiers

PMID41611768
PMCPMC12865011

What Socratic holds

Texttitle and abstract
LicenceCC BY
Read underepoch 390

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 Socratic graph.