Targeting IL-1 and TNF-α Receptors to Improve Cardiac Performance and Prevent Aortic Embolism in Venous Thrombosis
Thrombosis is a serious consequence of heart disease that can cause myocardial infarction, ischemic stroke, venous thromboembolism, and sudden death. Carrageenan-induced rats' tail vein thrombosis (VT) model is one that has been used experimentally to assess thrombolytic and antithrombotic medications. This work aimed to track the potential of VT to impact cardiac tissue, leading to myocardial infarction and aortic thrombosis, where IL-1 receptor antagonist type 1 (IL-1RA1) and TNF-α receptor antagonist type 2 (TNF-α RA2) were assessed as treating receptor blockers. Rats intraperitoneally injected with one dose of κ-carrageenan (20 mg/kg b. wt.). After 24 hours of induction, treatment with IL-1RA1 and TNF-α RA2 lasts for 7 days. The D-dimer level, lactate dehydrogenase (LDH), its isoenzymes and creatine kinase (CK), inflammatory marker (IL-6), intracellular adhesion molecule-1 (ICAM-1) and the histopathological features of heart tissue and aorta were evaluated. The results revealed significant elevation (p<0.001) in D-dimer, LDH, CK, IL-6 and ICAM-1 levels in thrombotic group. IL-1RA1 and TNF-α RA2 treatment improved the chosen parameters by variable degrees. IL-1RA1 had a stronger therapeutic effect than TNF-α RA2. Heart architectures were improved and a decline in aortic thrombus was noticed. In conclusion, IL-1RA1 showed promising therapeutic agent against VT, potentially reducing thrombus formation and lowering the risk of cardiovascular complications.
Authors
- Manal A. Hamed (ORCID: https://orcid.org/0000-0003-3643-5842)
- Yomna R. Ahmed
- Wagdy K. B. Khalil (ORCID: https://orcid.org/0000-0002-0598-7217)
- Asmaa F. Aboul Naser
Institutions
- National Research Centre (EG)
Publication Details
- Journal
- Egyptian Journal of Chemistry
- Published
- 2025-10-13
- DOI
- https://doi.org/10.21608/ejchem.2025.411704.12152
- Primary Topic
- Venous Thromboembolism Diagnosis and Management
- Type
- article
- Field-Weighted Citation Impact
- 0.00