Abstract

Background: Myocardial infarction (MI), a life-threatening disorder, arises from the imbalance between oxygen supply and myocardial demand. Linalool is a naturally occurring monoterpenes with proved numerous pharmacological actions. This study investigated the cardioprotective effect of Linalool on isoproterenol (ISO)-induced MI in rat models and explored part of the underlying molecular mechanisms. Methods: Rats were divided into five groups; groups I and II served as normal and linalool control groups, Group III administered ISO alone; groups V and VI received two different doses of Linalool and were challenged by ISO. Different biochemical parameters were determined, including hemodynamic, infarction size, cardiac enzymes, apoptotic markers, and inflammatory mediators. Results: Linalool limited the infarcted area size and diminished the elevated cardiac enzymes. Linalool escalated HO-1 and Nrf2, both nuclear and cytosol fractions, and reduced Keap 1. Linalool enhanced cardiac antioxidant activities, reduced inflammatory cytokines (tumor necrosis factor-alpha (TNF-α), nuclear factor-κ-B (NF-κB), interleukin 1 beta (IL-1β), interleukin 6 (IL-6)), apoptotic markers (Caspase-3, Caspase-9, and Bax), and elevated Bcl2. Conclusion: Linalool could act as an effective cardioprotective agent in the MI model through improving the oxidative condition, probably via the Nrf2/HO-1 pathway and by abolishing both apoptotic and inflammatory responses.

Highlights

  • Ischemic heart diseases (IHDs) are among the most threatening diseases to human life due to high rates of attack and associated disability and mortality

  • The main purpose of the current study is to explore the cardioprotective effect of the monoterpene alcohol, linalool, on Myocardial infarction (MI) through administrating the drug in ISO-induced MI rat models

  • Linalool represented 47.24% of the purified lavender volatile oil, an elevated percentage that was enough to encourage its isolation via column chromatography procedures (Figure 1a)

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Summary

Introduction

Ischemic heart diseases (IHDs) are among the most threatening diseases to human life due to high rates of attack and associated disability and mortality. Myocardial infarction (MI), a common presentation of IHD, is an acute disorder arising from an imbalance between oxygen supply and myocardium demand [1]. Under oxidative stress or other potentially damaging stimuli, Nrf dissociates from Keap in the cytoplasm and translocates into the nucleus, leading to the transcriptional activation of phase II enzymes/antioxidant genes, including HO-1, glutathione S transferase (GST), and glutamate cysteine ligase (GCL), etc. Different biochemical parameters were determined, including hemodynamic, infarction size, cardiac enzymes, apoptotic markers, and inflammatory mediators. Linalool enhanced cardiac antioxidant activities, reduced inflammatory cytokines (tumor necrosis factor-alpha (TNF-α), nuclear factor-κ-B (NF-κB), interleukin 1 beta (IL-1β), interleukin 6 (IL-6)), apoptotic markers (Caspase-3, Caspase-9, and Bax), and elevated Bcl. Conclusion: Linalool could act as an effective cardioprotective agent in the MI model through improving the oxidative condition, probably via the Nrf2/HO-1 pathway and by abolishing both apoptotic and inflammatory responses

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