Cardioprotective effect of ‘Marutham’ a polyherbal formulation on isoproterenol induced myocardial infarction in Wistar rats

Fitoterapia ◽  
2008 ◽  
Vol 79 (6) ◽  
pp. 433-438 ◽  
Author(s):  
Ponnian Stanely Mainzen Prince ◽  
Selvaraju Suman ◽  
Periyathambi Thangappan Devika ◽  
Muthukumarasamy Vaithianathan
Author(s):  
MYTHILY PANNEERSELVAM ◽  
DEVIKA P. T

Objective: This study aims to evaluate the cardioprotective effect of fisetin on change in the activities of lysosomal enzymes in isoproterenol (ISO)- induced myocardial infarction (MI) in male albino Wistar rats. Methods: Rats were orally pretreated with fisetin (30 mg/kg body weight) daily for 30 days. After the pretreatment period, ISO (100 mg/kg body weight) was subcutaneously administered to rats at intervals of 24 h for 2 consecutive days. Results: The activities of β-glucuronidase, β-N-acetylglucosaminidase, β-galactosidase, cathepsin-B, and cathepsin-D were significantly (*p<0.05) increased in serum and the heart of ISO-induced rats. Pre-treatment with fisetin daily for 30 days to ISO-induced rats significantly prevented these activities and restored their activities to near normal. Oral treatment with fisetin (30 mg/kg body weight) to normal control rats did not show any significant effect. Conclusion: We have concluded that fisetin protects the β-glucuronidase, β-N-acetylglucosaminidase, β-galactosidase, cathepsin-B, and cathepsin-D against ISO-induced MI. The observed effects might be due to the free radical-scavenging and membrane-stabilizing effect of fisetin.


2016 ◽  
Vol 11 (1) ◽  
pp. 231 ◽  
Author(s):  
Ravi Mundugaru ◽  
Padmaja Udaykumar ◽  
Sivanesan Senthilkumar ◽  
Sudhakara Bhat

<p>The present study reveals the protective effect of<em> Garcinia pedunculata</em> aqueous fruit extract in isoprenaline-induced myocardial infarction in Wistar rats. Isoprenaline (200 mg/kg) administration subcutaneous once daily for two consecutive days significantly (p&lt;0.01) increased the CK-MB, AST, ALT, ALP activity and CRP (p&lt;0.05) levels. Pretreatment with extract (400 mg/kg) orally for 14 consecutive days significantly ameliorated the effect of isoprenaline by reducing the activity of CK-MB and the levels of ALP, SGPT respectively. No significant changes were seen in the case of SGOT activity and CRP levels. Severe necrotic lesions in the myocardial tissue were observed in isoprenaline-treated group. In extract-treated group, mild degenerative changes of myo-cardial tissues to nearly normal cytoarchitecture were seen. The results indicate the cardioprotective effect of <em>G. pedunculata</em> against isoprenaline- induced myocardial infarction rat model.</p><p> </p>


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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