Why the study?
Linalool has demonstrated numerous pharmacological actions, but its cardioprotective effect and underlying molecular mechanisms in isoproterenol-induced MI remained to be investigated.
Does Linalool protect against isoproterenol-induced myocardial infarction in rat models?
Does Linalool protect against isoproterenol-induced myocardial infarction in rat models?
Linalool demonstrates cardioprotective effects in a rat model of isoproterenol-induced myocardial infarction by improving oxidative stress and reducing apoptosis and inflammation.
Linalool cardioprotection in rat MI model; hypothesis-generating with clinical translation untested.
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.
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Mohamed et al. (2021) studied this question.
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