scholarly journals Cardioprotective Effect of Ethanolic Extract of Leaves of Amaranthus cruentus in Isoprenaline-Induced Myocardial Infarction in Rats

2020 ◽  
Vol 10 (1) ◽  
pp. 24-28
Author(s):  
Priya Bisen ◽  
Aman Chaturvedi ◽  
Aditya Ganeshpurkar ◽  
Nazneen Dubey
2012 ◽  
Vol 141 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Althaf Hussain Shaik ◽  
S.N. Rasool ◽  
A. Vikram Kumar Reddy ◽  
M. Abdul Kareem ◽  
G. Saayi Krushna ◽  
...  

Life ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 120
Author(s):  
Maged E. Mohamed ◽  
Mohamed S. Abduldaium ◽  
Nancy S. Younis

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.


2015 ◽  
Vol 33 (3) ◽  
pp. 109-117 ◽  
Author(s):  
Guo-Long Gu ◽  
Xiao-Lin Xu ◽  
Xiao-Tian Sun ◽  
Ji Zhang ◽  
Chang-Fa Guo ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Ramón Rodrigo ◽  
Matías Libuy ◽  
Felipe Feliú ◽  
Daniel Hasson

Acute myocardial infarction (AMI) is the leading cause of mortality worldwide. Major advances in the treatment of acute coronary syndromes and myocardial infarction, using cardiologic interventions, such as thrombolysis or percutaneous coronary angioplasty (PCA) have improved the clinical outcome of patients. Nevertheless, as a consequence of these procedures, the ischemic zone is reperfused, giving rise to a lethal reperfusion event accompanied by increased production of reactive oxygen species (oxidative stress). These reactive species attack biomolecules such as lipids, DNA, and proteins enhancing the previously established tissue damage, as well as triggering cell death pathways. Studies on animal models of AMI suggest that lethal reperfusion accounts for up to 50% of the final size of a myocardial infarct, a part of the damage likely to be prevented. Although a number of strategies have been aimed at to ameliorate lethal reperfusion injury, up to date the beneficial effects in clinical settings have been disappointing. The use of antioxidant vitamins could be a suitable strategy with this purpose. In this review, we propose a systematic approach to the molecular basis of the cardioprotective effect of antioxidant vitamins in myocardial ischemia-reperfusion injury that could offer a novel therapeutic opportunity against this oxidative tissue damage.


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