Please use this identifier to cite or link to this item: http://dspace.sctimst.ac.in/jspui/handle/123456789/197
Title: Cardoguard, an Ayurvedic antihypertensive formulation, prevents cardiac remodeling in spontaneously hypertensive rats by inhibition of ERK and PKC epsilon signaling pathways
Authors: Sankar, Vandana
Nair, Renuka R.
Harikrishnan, Vijayakumar S.
Fernandez, Adelaide C.
Kumar, Cherumanal S. Krishna
Madhavachandran, Viswanathamenon
Keywords: Experimental Medicine
Issue Date: 2012
Publisher: CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
Citation: CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY. 90; 5; 627-635
Abstract: Ayurveda is an Indian system of medicine. Despite clinical efficacy, lack of scientific validation has limited the effective use of Ayurvedic drugs. Cardoguard is an Ayurvedic antihypertensive drug formulated by Nagarjuna Herbal Concentrates Ltd., Kerala, India. Left ventricular hypertrophy (LVH) is a modifiable risk factor, and regression of LVH reduces the propensity for adverse cardiovascular events. This study was taken up with the objective of evaluating the efficacy of Cardoguard in the prevention of cardiac remodeling. Cardoguard was administered orally to 2-month-old spontaneously hypertensive rats for 4 months at a dose of 5 mg.day(-1). The dose corresponds to the therapeutic dose calculated on the basis of body surface area. Lower hypertrophy index, decrease in cardiomyocyte area, and reduction of interstitial fibrosis in treated spontaneously hypertensive rats indicate amelioration of cardiac hypertrophy by Cardoguard. Cardiac output increased in response to treatment. Immunostaining for the phosphorylated components of major signaling pathways associated with hypertrophy suggests that prevention of LVH by Cardoguard is possibly mediated through inhibition of extracellular signal-regulated kinases and protein kinase C-3 signaling pathways. Reduced expression of 3-nitrotyrosine in response to the treatment suggests that prevention of cardiac remodeling by Cardoguard is mediated by reduction of oxidative stress.
URI: http://dx.doi.org/10.1139/Y2012-047
http://dspace.sctimst.ac.in/jspui/handle/123456789/197
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