Journals / Eurasian Journal of Medical Investigation / 2022 / Cilt: 6 - Sayı: 2

Could ARNI have an Effect on LV Fibrosis and Inflammatory Parameters in an Experimental Autoimmune Myocarditis Model?

Pages
190–197
Publication Date
2022-10-12
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Studies to be conducted in high-numbered groups will reveal more statistical significance.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objectives: The aim of this study is to investigate the efficacy of sacubitril-valsartan treatment in the early period of Experimental Autoimmune Myocarditis (EAM) model, under the perspective of fibrosis and inflammatory cytokines.
📊
Key Findings & Data:Methods: The study was performed using 18 rats in three groups of EAM (n=6), EAM treatment (n=6) and control (n=6).
💡
Conclusion & Impact:Studies to be conducted in high-numbered groups will reveal more statistical significance.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objectives: The aim of this study is to investigate the efficacy of sacubitril-valsartan treatment in the early period of Experimental Autoimmune Myocarditis (EAM) model, under the perspective of fibrosis and inflammatory cytokines. Methods: The study was performed using 18 rats in three groups of EAM (n=6), EAM treatment (n=6) and control (n=6). EAM was induced by footpad injections of porcine cardiac myosin and Complete Freund’s Adjuvant (CFA). The EAM group was not given any medical care. 20 mg/kg sacubitril-valsartan was given to EAM treatment (marked as treatment) group twice a day beginning from the 21st day to the 42nd day. No procedure was applied to the control group. Histopathological, biochemical and RT-PCR analyses were performed on the heart tissues taken after the 42nd day of sacrificing. Results: Significant congestion, fibrosis, and cellular changes were observed in the EAM and treatment groups. There was 50% less severe fibrosis,which is 3rd degree, in the Treatment group compared to EAM. Severe congestion rate was lower in the treatment group compared to EAM; with the percentage of 16,6% to 50%. Though the average values of treatment group were lower than EAM group, there was obvious difference in TNF α, TGF β1 and NT-proBNP levels (p>0.05) between the EAM and the treatment groups. There was no significant difference in IL-6 levels between the three groups. Conclusion: In view of findings, the treatment of ARNI in acute autoimmune myocarditis may be promising on cardiac risk markers (cytokine, BNP values) and fibrosis parameters. Studies to be conducted in high-numbered groups will reveal more statistical significance.

🔖

Cite This Article

ÖZTOPUZ, R. Ö., DEVECİ, B., DUYGU, A., ADALI, Y., GAZİ, E., ARSLAN, M. (2022). Could ARNI have an Effect on LV Fibrosis and Inflammatory Parameters in an Experimental Autoimmune Myocarditis Model?. Eurasian Journal of Medical Investigation, Cilt: 6 - Sayı: 2, 190–197. https://ajindex.com/articles/508546

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (14)

  1. Fung G, Luo H, Qiu Y, Yang D, McManus B. Myocarditis. Circ Res 2016;118:496–514
  2. Felker GM, Boehmer JP, Hruban RH, Hutchins GM, Kasper EK, Baughman KL, et al. Echocardiographic findings in fulminant and acute myocarditis. J Am Coll Cardiol 2000;36:227–32
  3. Global Burden of Disease Study 2013 Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet 2015;386:743– 800
  4. Jared W. Magnani and G. William Dec. Myocarditis current trends in diagnosis and treatment. Circulation Research 2006;113:876–90
  5. Blyszczuk P, Müller-Edenborn B, Valenta T, Osto E, Stellato M, Behnke S, et al. Transforming growth factor-β-dependent Wnt secretion controls myofibroblast formation and myocardial fibrosis progression in experimental autoimmune myocarditis. Eur Heart J 2017;38:1413–25
  6. Liu G, Ma C, Yang H, Zhang PY. Transforming growth factor β and its role in heart disease. Exp Ther Med 2017;13:2123–8
  7. Rosenkranz S. TGF-beta1 and angiotensin networking in cardiac remodeling. Cardiovasc Res 2004;63:423–32
  8. Schultz Jel J, Witt SA, Glascock BJ, Nieman ML, Reiser PJ, Nix SL, et al. TGF-beta1 mediates the hypertrophic cardiomyocyte growth induced by angiotensin II. J Clin Invest 2002;109:787– 96
  9. Gu J, Noe A, Chandra P, Al-Fayoumi S, Ligueros-Saylan M, Sarangapani R, et al. Pharmacokinetics and pharmacodynamics of LCZ696, a novel dual-acting angiotensin receptor-neprilysin inhibitor. J Clin Pharmacol 2010;50:401–14
  10. Gardner DG, Chen S, Glenn DJ, Grigsby CL. Molecular biology of the natriuretic peptide system: implications for physiology and hypertension. Hypertension 2007;49:419–26
  11. Eriksson U, Kurrer MO, Schmitz N, Marsch SC, Fontana A, Eugster HP, et al. Interleukin- 6-deficient mice resist development of autoimmune myocarditis associated with impaired upregulation of complement C3. Circulation 2003;107:320–5
  12. Milenković M, Arsenović-Ranin N, Stojić-Vukanić Z, Bufan B, Vučićević D, Jančić I. Quercetin ameliorates experimental autoimmune myocarditis in rats. J Pharm Pharm Sci 2010;13:311–9
  13. Godsel LM, Leon JS, Wang K, Fornek JL, Molteni A, Engman DM. Captopril prevents experimental autoimmune myocarditis. J Immunol 2003;171:346–52
  14. Suematsu Y, Miura S, Goto M, Matsuo Y, Arimura T, Kuwano T, et al. LCZ696, an angiotensin receptor-neprilysin inhibitor