# Empagliflozin and platelet-rich plasma improve stanozolol induced cardiotoxicity by reducing NF-κB/P65, IL-1B and apoptosis

**Authors:** Shaimaa M. Hafez, Eman Mohammed Elsaeed, Amal Hussain Mohammed Ali, Eman S. Said, Yara S. Abouelela, Asmaa Abdo Elshiech, Heba Abdelnaser Aboelsoud, Hala Magdy Anwer, Samar H. Elsharkawy, Marwa A. Ibrahim, Hamdy Rizk, Hoda A. Abd-Ellatieff

PMC · DOI: 10.1186/s40360-026-01086-3 · BMC Pharmacology & Toxicology · 2026-02-23

## TL;DR

This study shows that Empagliflozin and platelet-rich plasma can reduce heart damage caused by stanozolol in rats by lowering inflammation and cell death.

## Contribution

The study introduces Empagliflozin and PRP as potential treatments for stanozolol-induced cardiotoxicity.

## Key findings

- Stanozolol caused oxidative stress and inflammation in rat hearts.
- Empagliflozin and PRP reduced markers of inflammation and apoptosis.
- Treatments improved structural and functional heart health in affected rats.

## Abstract

Stano is an anabolic androgenic steroid (AAS) with various adverse cardiovascular effects because it induces ventricular dysfunction. The objective of this study was to evaluate and demonstrate how Empagliflozin (EP) and platelet-rich plasma (PRP) can reduce the cardiotoxic effects linked to Stano administration in albino rats.

Fifty-four (n = 54) rats were involved in this research, the animals were randomly divided into six groups: (C, EP, PRP, Stano, SEP, and SPRP). Various cardiovascular health markers, focusing on the relationship between oxidative stress and inflammation in cardiomyopathy were evaluated.

There was extensive myocardial injury and damage in the Stano group, as reflected by induction of oxidative stress by increase in the level of MDA, along with significantly reduced level of GSH and CAT. Increased expression of inflammatory markers like IL-1β, and NF-κB/P65 pathway, with strong immunoreactivity of caspase-3-an apoptosis marker in cardiac tissue were observed. Evidence of left ventricular hypertrophy with pathological changes in cardiac tissues was also noted, together with functional impairments. Hypertrophy acts as a compensatory mechanism against injury and stress, since it may cause various complications in case of a lack of intervention.

Stano activates the initiation of some apoptotic and inflammatory signaling pathways to cause serious aggravated cardiovascular health threats. On the other hand, all the structural function and antioxidant parameters related to cardiovascular health showed improvement after both EP and PRP treatments. Intriguingly, EP and PRP have emerged as effective promising agents against the deleterious cardiac damage linked to Stano use. Nevertheless, more research is actually needed to explain the mechanisms and optimize clinical application or management of those exposed to ASS.

## Linked entities

- **Proteins:** IL1B (interleukin 1 beta), Casp3 (caspase 3)
- **Chemicals:** Empagliflozin (PubChem CID 11949646), stanozolol (PubChem CID 25249), MDA (PubChem CID 1614), GSH (PubChem CID 124886)
- **Diseases:** cardiomyopathy (MONDO:0004994)

## Full-text entities

- **Genes:** NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, RELA (RELA proto-oncogene, NF-kB subunit) [NCBI Gene 5970] {aka AIF3BL3, CMCU, NFKB3, p65}
- **Diseases:** cardiotoxicity (MESH:D066126)
- **Chemicals:** Empagliflozin (MESH:C570240), stanozolol (MESH:D013197)

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12990588/full.md

## References

5 references — full list in the complete paper: https://tomesphere.com/paper/PMC12990588/full.md

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Source: https://tomesphere.com/paper/PMC12990588