Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/13645
Title: Effects of phikud navakot extract on myocardial ischemia/reperfusion injury in rats
Authors: Kengkoom K.
Sirimontaporn A.
Sotanaphun U.
Gerdprasert O.
Nusuetrong P.
Keywords: heme oxygenase 1
lactate dehydrogenase
mitogen activated protein kinase
nitrous oxide
Phikud navakot extract
plant extract
protein kinase B
troponin I
unclassified drug
phikud navakot
plant extract
adult
animal experiment
animal model
animal tissue
Article
blood sampling
controlled study
coronary artery ligation
electrocardiography
heart muscle injury
heart muscle ischemia
heart protection
histopathology
immunoassay
left coronary artery
male
nonhuman
protein expression
rat
ST segment elevation
upregulation
Western blotting
animal
chemistry
heart muscle
medicinal plant
Myocardial Reperfusion Injury
pathology
Sprague Dawley rat
Animals
Electrocardiography
Male
Myocardial Reperfusion Injury
Myocardium
Plant Extracts
Plants, Medicinal
Rats
Rats, Sprague-Dawley
Issue Date: 2015
Abstract: Background: Phikud Navakot (PN) is a set of nine medicinal plants and the main ingredient of “Yahom Navakot”, a traditional Thai herbal formula for treatment of cardiovascular symptoms. Objective: To investigate the cardioprotective effects of PN on myocardial ischemia/reperfusion (IR) in male Sprague Dawley rats. Material and Method: Rats were randomly divided into 7 groups: sham, IR, and IR orally pretreated with PN (10, 50, 100, 200, and 400 mg/kg BW) for 7 days. After treatment, IR induction was performed by left coronary artery (LCA) ligation for 30 min, followed by reperfusion for 24 h. At the end of the experiment, blood was collected for hematological and biochemical parameters, and hearts were immediately removed for histopathological examination and Western blot analysis. Results: IR induction caused ST elevation in the electrocardiogram and an increase in serum troponin I (TnI), confirming myocardial damage. In addition, histopathological changes of ischemic myocardium showed inflammation, infiltration, and edema. Oral administration of PN (10, 50, 100, 200, and 400 mg/kg BW) for 7 days prior to IR simulation showed no change on serum TnI and histopathology of cardiac tissues, when compared to IR group. However, Western blot analysis showed that IR rats pretreated with PN (10 mg/kg BW) significantly increased (p<0.05) pERK/ERK ratio, meanwhile pretreated with PN (50-200 mg/kg BW) up-regulated (p<0.05) the protein expression of HO-1, when compared with IR group. Conclusion: The present study implied that 7-day pretreatment of PN failed to protect cardiac tissues against IR injury induced by LCA ligation. Investigation at molecular level found however that PN up-regulated the expression of protective proteins pERK/ERK ratio and HO-1 in cardiac tissues, suggesting molecular mechanism of PN in cardioprotection against IR injury. © 2015, Medical Association of Thailand. All rights reserved.
URI: https://ir.swu.ac.th/jspui/handle/123456789/13645
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84957616565&partnerID=40&md5=561dd6ef35cb131e62053d21acb13c5e
ISSN: 1252208
Appears in Collections:Scopus 1983-2021

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