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Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
Published on: August 16, 2019
Myocardial expression of TNF-alpha, IL-1beta, IL-6, IL-8, IL-10 and MCP-1 after a single MDMA dose administered in a
Margherita Neri1, Stefania Bello, Alessandro Bonsignore
1Department of Forensic Pathology, University of Foggia, Ospedale Colonnello D'Avanzo, 71100 Foggia, Italy.
Abstract:
Indirect effects of 3,4-methylenedioxy-N-methylamphetamine (MDMA) and metabolites on the cardiac cells are well-known, the mechanism(s) underlying direct MDMA-induced cardiotoxicity remaining to be clarified. To better understand the immuno-inflammatory phenomena accompanying the cardiac alterations during MDMA administration, we conducted a study in an in vivo animal model to evaluate the cellular morphological alterations related to the biological response between MDMA administration and inflammatory cytokines (tumor necrosis factor-alpha, IL-1beta, IL-6, 8, 10, and monocyte chemotactic protein-1). A total of 25 male rats were used. The effects were evaluated at 6, 16 and 24 hours after a single dose MDMA administered (20 mg/kg i.p.). We found high levels of the cardioinhibitory cytokines in rat heart after 3 and 6 hs from MDMA administration. Strongest reaction was observed at 24 hs for TNF-alpha, IL-1beta, IL-6, 8, 10 and for MCP-1. Furthermore, we still determined the presence of MDMA and MDA in the plasma of rats treated with MDMA intra-peritoneal single injection; it was present as early at 6 hs and still present 24 hs after treatment. Western blot analysis in cardiac samples demonstrated the IL-1beta and IL-6 reactions in rats died spontaneously at fourth hour. The rise of the selective cardioinhibitory cytokines may be interpreted as the adaptive response of jeopardized myocardium to the cardiac dysfunction resulting from MDMA injection.
Insights
This study investigated the direct cardiotoxicity of 3,4-methylenedioxy-N-methylamphetamine (MDMA) in rats. MDMA administration led to increased cardioinhibitory cytokines in the heart, suggesting an adaptive response to cardiac dysfunction.
Area of Science:
- Cardiovascular Toxicology
- Neuropharmacology
- Immunology
Background:
- Direct mechanisms of 3,4-methylenedioxy-N-methylamphetamine (MDMA) cardiotoxicity are not fully understood.
- MDMA's indirect effects on cardiac cells are known, but direct cellular damage pathways require clarification.
- Investigating the link between MDMA exposure and inflammatory responses in the heart is crucial.
Purpose of the Study:
- To explore the immuno-inflammatory phenomena associated with MDMA-induced cardiac alterations.
- To evaluate cellular morphological changes in response to MDMA administration and inflammatory cytokines.
- To determine the time course of MDMA and its metabolites in plasma and their correlation with cardiac inflammatory markers.
Main Methods:
- An in vivo study using 25 male rats exposed to a single dose of MDMA (20 mg/kg i.p.).
- Evaluation of cellular morphology and inflammatory cytokine levels (TNF-alpha, IL-1beta, IL-6, IL-8, IL-10, MCP-1) at 6, 16, and 24 hours post-administration.
- Detection of MDMA and MDA in plasma via analytical methods.
- Western blot analysis of cardiac samples for IL-1beta and IL-6 in rats that died spontaneously.
Main Results:
- Elevated levels of cardioinhibitory cytokines were observed in rat hearts 3-6 hours after MDMA administration.
- Peak inflammatory response, including TNF-alpha, IL-1beta, IL-6, IL-8, IL-10, and MCP-1, was noted at 24 hours.
- MDMA and its metabolite MDA were detected in rat plasma from 6 to 24 hours post-injection.
- Western blot confirmed IL-1beta and IL-6 presence in cardiac tissue of rats that died within 4 hours.
Conclusions:
- The observed increase in cardioinhibitory cytokines suggests an adaptive response of the myocardium to MDMA-induced cardiac dysfunction.
- MDMA administration triggers a significant immuno-inflammatory cascade in cardiac tissue.
- The findings highlight the complex interplay between MDMA, cardiac function, and inflammatory pathways.
