Cardioprotective Effect of Linalool against Isoproterenol-Induced Myocardial Infarction

被引:19
|
作者
Mohamed, Maged E. [1 ,2 ]
Abduldaium, Mohamed S. [3 ]
Younis, Nancy S. [1 ,4 ]
机构
[1] King Faisal Univ, Dept Pharmaceut Sci, Coll Clin Pharm, Al Hasa 31982, Saudi Arabia
[2] Zagazig Univ, Dept Pharmacognosy, Coll Pharm, Zagazig 44519, Egypt
[3] Zagazig Univ, Dept Cardiol, Coll Med, Zagazig 44519, Egypt
[4] Zagazig Univ, Dept Pharmacol, Zagazig 44519, Egypt
来源
LIFE-BASEL | 2021年 / 11卷 / 02期
关键词
apoptosis; essential oils; inflammatory markers; ischemic heart disease; monoterpene alcohols;
D O I
10.3390/life11020120
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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-alpha), nuclear factor-kappa-B (NF-kappa B), interleukin 1 beta (IL-1 beta), 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.
引用
收藏
页码:1 / 17
页数:17
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