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D-Limonene mitigate myocardial injury in rats through MAPK/ERK/NF-κB pathway inhibition
1Department of Pharmaceutical Sciences, College of Clinical Pharmacy, King Faisal University, Al-Hasa 31982, Kingdom of Saudi Arabia.
Abstract:
Cardiovascular diseases are the primary reason of mortality, among which myocardial infarction (MI) is the most dominant and prevalent. This study was considered to examine D-Limonene protective action against isoproterenol (ISO) induced MI. Wister male rats were dispersed into four groups. Normal and D-Limonene control group in which rats administered saline or D-Limonene. ISO control animals were administered saline for 21 days then challenged with ISO (85 mg/kg, subcutaneously) on 20th and 21st day for MI induction. D-Limonene pretreated group in which animals were pretreated with D-Limonene 50 mg/kg orally for 21 days then administered ISO on 20th and 21st day. MI prompted variations were assessed by myocardial infarction area determination, blood pressure (BP) alterations, cardiac injury biomarkers and inflammatory mediators measurements. For more depth investigation, both the apoptotic status was evaluated via measuring mRNA expression of Bcl-2 and Bax as well as mitogen-activated protein kinase-extracellular signal-regulated kinase (MAPK-ERK) signal transduction were investigated via Western blotting. MI group revealed significant infarcted area, blood pressure alterations, myocardial injury enzymes intensification together with inflammatory cytokines amplification. MI was associated with activation of MAPK-ERK signal pathway and apoptotic status within the myocardium. On the other hand, pretreated with D-Limonene demonstrated deterred infracted area, reduced myocardial enzymes, improved BP indices, lessened inflammatory levels. Furthermore, D-Limonene pretreatment caused a decline in MAPK proteins pathway and Bax relative mRNA expression, while intensifying Bcl-2 mRNA expression promoting that D-Limonene may constrain MI induced myocardial apoptosis. D-Limonene mitigated MI injury through MAPK/NF-κB pathway inhibition and anti-apoptotic effect.
Insights
D-Limonene protects against heart attacks by reducing inflammation and cell death. This study shows D-Limonene can prevent myocardial infarction (MI) damage in rats.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background:
- Cardiovascular diseases, particularly myocardial infarction (MI), are a leading cause of mortality worldwide.
- Isoproterenol (ISO) is commonly used to induce experimental MI in animal models for research purposes.
- Understanding protective agents against MI is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the protective effects of D-Limonene against isoproterenol (ISO)-induced myocardial infarction (MI) in Wistar male rats.
- To elucidate the molecular mechanisms underlying D-Limonene's cardioprotective action, focusing on apoptosis and MAPK-ERK signaling.
- To assess the impact of D-Limonene on cardiac injury biomarkers and inflammatory mediators.
Main Methods:
- Rats were divided into four groups: normal control, D-Limonene control, ISO control, and D-Limonene pretreated + ISO.
- Myocardial infarction was induced by subcutaneous ISO injection on days 20 and 21.
- D-Limonene (50 mg/kg) was administered orally for 21 days in the pretreatment group.
- Assessments included infarct size, blood pressure, cardiac enzymes, inflammatory cytokines, Bcl-2/Bax mRNA expression, and MAPK-ERK pathway activation via Western blotting.
Main Results:
- ISO-induced MI resulted in significant myocardial damage, elevated cardiac enzymes, increased blood pressure, and amplified inflammatory cytokines.
- MI triggered the activation of the MAPK-ERK signaling pathway and induced apoptosis in the myocardium.
- D-Limonene pretreatment significantly reduced infarct area, improved blood pressure, decreased cardiac injury markers, and lowered inflammatory levels.
- D-Limonene inhibited MAPK protein expression and Bax mRNA, while upregulating Bcl-2 mRNA, indicating an anti-apoptotic effect.
Conclusions:
- D-Limonene exhibits significant cardioprotective effects against ISO-induced myocardial infarction in rats.
- The protective mechanism involves the inhibition of the MAPK/NF-κB pathway and suppression of myocardial apoptosis.
- D-Limonene demonstrates potential as a therapeutic agent for mitigating myocardial infarction injury.
