Gupta V.K.,Rajendra Institute of Technology and science |
Sharma S.K.,Guru Jambheshwar University of Science and Technology
Indian Journal of Natural Products and Resources | Year: 2014
Oxygen free radicals induce damage due to peroxidation to biomembranes and also to DNA, which lead to tissue damage, thus cause occurrence of a number of diseases. Antioxidants neutralise the effect of free radicals through different ways and may prevent the body from various diseases. Antioxidants may be synthetic or natural. Synthetic antioxidants such as butylated hydroxytoluene (BHT) and butylated hydroxyanisole (BHA) have recently been reported to be dangerous for human health. Thus, the search for effective, non-toxic natural compounds with antioxidative activity has been intensified in recent years. The present review includes a brief account of research reports on plants with antioxidant potential. © 2014, National Institute of Science Communication and Information Resources (NISCAIR). All rights reserved.
Dorwal D.,Rajendra Institute of Technology and science
International Journal of Pharmacy and Technology | Year: 2012
The purpose of this research work was to develop and evaluate transdermal therapeutic system containing Methyl salicylate with different polymeric combinations by the solvent evaporation technique. Five transdermal patch formulations (F1, F2, F3, F4 and F5) consists of HPMC and PVP were prepared. All formulations carried menthol as penetration enhancer and glycerin as plasticizer. The prepared transdermal patches were evaluated for in vitro release, moisture absorption, moisture loss and other physico-chemical properties. The diffusion studies were performed by using modified Franz diffusion cells. The formulation, F5 showed maximum release of 95.72±1.07% in 24 h, followed Higuchi kinetics and the mechanism of release was diffusion mediated.
Balakumar P.,Rajendra Institute of Technology and science |
Taneja G.,Rajendra Institute of Technology and science
Free Radical Biology and Medicine | Year: 2012
Fish oil is recommended for the management of hypertriglyceridemia and to prevent secondary cardiovascular disorders. Fish oil is a major source of ω-3-polyunsaturated fatty acids (PUFAs) such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Clinical studies suggest that fish oil not only prevents the incidence of detrimental cardiovascular events, but also lowers the cardiovascular mortality rate. In addition to a classic lipid-lowering action, ω-3-PUFAs in fish oil could regulate blood pressure and enhance vascular integrity and compliance. Additionally, ω-3-PUFAs have the ability to protect vascular endothelial cells by decreasing oxidative stress, halting atherosclerotic events, and preventing vascular inflammatory and adhesion cascades. Intriguingly, recent studies have demonstrated that ω-3-PUFAs improve the function of vascular endothelium by enhancing the generation and bioavailability of endothelium-derived relaxing factor (nitric oxide) through upregulation and activation of endothelial nitric oxide synthase (eNOS). This certainly opens up a new area of research identifying potential mechanisms influencing fish oil-mediated functional regulatory action on vascular endothelium. We address in this review the potential of fish oil to prevent vascular endothelial dysfunction and associated cardiovascular disorders. Moreover, the mechanisms pertaining to fish oil-mediated eNOS activation and nitric oxide generation in improving endothelial function are delineated. We finally suggest the importance of further studies to determine the dose adjustment of fish oil with an optimal ratio of EPA and DHA for achieving consistent cardiovascular protection. © 2012 Elsevier Inc.
Bhardwaj P.,Rajendra Institute of Technology and science |
Khanna D.,Rajendra Institute of Technology and science
Chinese Journal of Natural Medicines | Year: 2013
Green tea, Camellia sinensis (Theaceae), a major source of flavonoids such as catechins, has recently shown multiple cardiovascular health benefits through various experimental and clinical studies. These studies suggest that green tea catechins prevent the incidence of detrimental cardiovascular events, and also lower the cardiovascular mortality rate. Catechins present in green tea have the ability to prevent atherosclerosis, hypertension, endothelial dysfunction, ischemic heart diseases, cardiomyopathy, cardiac hypertrophy and congestive heart failure by decreasing oxidative stress, preventing inflammatory events, reducing platelet aggregation and halting the proliferation of vascular smooth muscle cells. Catechins afford an anti-oxidant effect by inducing anti-oxidant enzymes, inhibiting pro-oxidant enzymes and scavenging free radicals. Catechins present anti-inflammatory activity through the inhibition of transcriptional factor NF-κB-mediated production of cytokines and adhesion molecules. Green tea catechins interfere with vascular growth factors and thus inhibit vascular smooth muscle cell proliferation, and also inhibit thrombogenesis by suppressing platelet adhesion. Additionally, catechins could protect vascular endothelial cells and enhance vascular integrity and regulate blood pressure. In this review various experimental and clinical studies suggesting the role of green tea catechins against the markers of cardiovascular disorders and the underlying mechanisms for these actions are discussed. © 2013 China Pharmaceutical University.
Sharma A.K.,Rajendra Institute of Technology and science |
Khanna D.,Rajendra Institute of Technology and science
Cellular Signalling | Year: 2013
Diabetes mellitus, a chronic metabolic disorder, is recognized as a root cause of cardiovascular disorders. A long-term and uncontrolled diabetes mellitus coincides with the cardiovascular signalling alteration, resulting in inadequacy of maintaining the cardiovascular physiology. Nitric oxide (NO) is an imperative mediator of cardiovascular physiology as its signalling is known to mediate vasodilatory, anti-platelet, anti-proliferative, and anti-inflammatory actions in vessels. In 1998, Robert Furchgott, Louis Ignarro and Ferid Murad received the Nobel Prize in Medicine or Physiology for their great discoveries concerning the role of NO (originally identified as endothelium-derived relaxing factor, EDRF) as a key signalling molecule in regulating cardiovascular physiology. The activation of phosphatidylinositol 3-kinase (PI3-K) further activates protein kinase B (PKB/Akt), which subsequently enhances eNOS activation and vascular NO generation. However, in recent studies a marked impairment in PI3-K/Akt-eNOS-NO signalling has been demonstrated in the condition of diabetes mellitus. Therefore, the defective PI3-K-Akt-eNOS-NO signalling pathways could make diabetic patients more vulnerable to cardiovascular disease pathology concerning the key functions of NO. Adenosine produced by cardiac cells has abilities to attenuate the proliferation of cardiac fibroblasts, inhibit collagen synthesis, and defend the myocardium against ischemia-reperfusion injury. However, diabetes mellitus is associated with enhanced unidirectional uptake of interstitial adenosine and reduced ability to release adenosine by cardiac cells during ATP deprivation. The reduced myocardial extracellular availability and increased uptake of adenosine could make diabetic subjects more susceptible to myocardial abnormalities. This review throws lights on diabetes mellitus-associated cardiovascular signalling alterations and their possible contribution to cardiovascular disease pathology. © 2013 Elsevier Inc.