scholarly journals Anti-HMG-CoA Reductase, Antioxidant, and Anti-Inflammatory Activities ofAmaranthus viridisLeaf Extract as a Potential Treatment for Hypercholesterolemia

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Shamala Salvamani ◽  
Baskaran Gunasekaran ◽  
Mohd Yunus Shukor ◽  
Noor Azmi Shaharuddin ◽  
Mohd Khalizan Sabullah ◽  
...  
Keyword(s):  
Leaf Extract ◽  
Cholesterol Metabolism ◽  
Inhibitory Effect ◽  
Hmg Coa Reductase ◽  
Synthetic Drugs ◽  
Reductase Inhibitors ◽  
Plot Analysis ◽  
Hmg Coa Reductase Inhibitors ◽  
Anti Inflammatory ◽  
Coa Reductase

Inflammation and oxidative stress are believed to contribute to the pathology of several chronic diseases including hypercholesterolemia (elevated levels of cholesterol in blood) and atherosclerosis. HMG-CoA reductase inhibitors of plant origin are needed as synthetic drugs, such as statins, which are known to cause adverse effects on the liver and muscles.Amaranthus viridis(A. viridis) has been used from ancient times for its supposedly medically beneficial properties. In the current study, different parts ofA. viridis(leaf, stem, and seed) were evaluated for potential anti-HMG-CoA reductase, antioxidant, and anti-inflammatory activities. The putative HMG-CoA reductase inhibitory activity ofA. viridisextracts at different concentrations was determined spectrophotometrically by NADPH oxidation, using HMG-CoA as substrate.A. viridisleaf extract revealed the highest HMG-CoA reductase inhibitory effect at about 71%, with noncompetitive inhibition in Lineweaver-Burk plot analysis. The leaf extract showed good inhibition of hydroperoxides, 2,2-diphenyl-1-picrylhydrazyl (DPPH), nitric oxide (NO), and ferric ion radicals in various concentrations.A. viridisleaf extract was proven to be an effective inhibitor of hyaluronidase, lipoxygenase, and xanthine oxidase enzymes. The experimental data suggest thatA. viridisleaf extract is a source of potent antioxidant and anti-inflammatory agent and may modulate cholesterol metabolism by inhibition of HMG-CoA reductase.

Statins and Inflammation in Cardiovascular Disease

2018 ◽  
Vol 23 (46) ◽  
pp. 7027-7039 ◽  
Author(s):  
Georgia Vogiatzi ◽  
Evangelos Oikonomou ◽  
Gerasimos Siasos ◽  
Sotiris Tsalamandris ◽  
Alexandros Briasoulis ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Lipid Lowering ◽  
Hmg Coa Reductase ◽  
Ample Evidence ◽  
Reductase Inhibitors ◽  
Immune System Activation ◽  
Hmg Coa Reductase Inhibitors ◽  
Anti Inflammatory ◽  
Artery Disease ◽  
Coa Reductase

Background: Chronic inflammation and immune system activation underlie a variety of seemingly unrelated cardiac conditions including not only atherosclerosis and the subsequent coronary artery disease but also peripheral artery disease, hypertension with target organ damage and heart failure. The beneficial effects of HMG-CoA reductase inhibitors or statins are mainly attributed to their ability to inhibit hepatic cholesterol biosynthesis. Beyond their lipid lowering activity, ample evidence exists in support of their potent anti-inflammatory properties which initiate from the inhibition of GTPase isoprenylation, activating a cataract of secondary pathways and extend to the inhibition and blocking of immune cell activation and interaction. </P><P> Objective: To summarize the anti-inflammatory mechanisms of statins in clinical and experimental settings in cardiovascular disease. </P><P> Methods: A systematic search of PubMed and the Cochrane Database was conducted in order to identify the majority of trials, studies, current guidelines and novel articles related to the subject. </P><P> Results: In vitro, statins have immuno-modulatory and anti-inflammatory effects, and they can exert antiatherosclerotic effects independently of their hypolipidemic actions. In addition, positive results have emerged from mechanistic and experimental studies on the active role of HMG-CoA reductase inhibitors in HF. By extrapolating those data in clinical setting, we further understand how HMG-CoA reductase inhibitors can beneficially affect not only systolic but also diastolic HF. </P><P> Conclusion: In this review article, we present the basic pathophysiologic data supporting the anti-inflammatory actions of statins in clinical and experimental settings and we link these mechanisms with confirmatory clinical data on the potent non lipid lowering effects of HMG-CoA reductase inhibitors.

HMG CoA reductase inhibitors affect Na(+)-H+ antiport activity in human lymphoblasts

1991 ◽  
Vol 261 (5) ◽  
pp. C780-C786 ◽  
Author(s):  
L. L. Ng ◽  
J. E. Davies
Keyword(s):  
Intracellular Ph ◽  
Inhibitory Effect ◽  
Hmg Coa Reductase ◽  
Reductase Inhibitors ◽  
Hmg Coa Reductase Inhibitors ◽  
Acid Load ◽  
Membrane Bound ◽  
Osmotic Stimulus ◽  
Coa Reductase ◽  
Intracellular Acid

The Na(+)-H+ antiport is a membrane-bound glycoprotein that extrudes intracellular acid loads and regulates cellular volume. Cellular synthesis of the oligosaccharide side chains of glycoproteins is dependent on a supply of mevalonate, itself a product of the rate-limiting enzyme of cholesterol synthesis 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase. The effect of two HMG CoA reductase inhibitors (simvastatin and 25-hydroxycholesterol) on intracellular pH and Na(+)-H+ exchange was therefore studied. Inhibition of the Na(+)-H+ antiport by these agents led to a fall in intracellular pH but did not impair the regulatory volume increase response to a hypertonic stimulus. The inhibitory effect of simvastatin was prevented by mevalonate but not dolichol or squalene. The effect of 25-hydroxycholesterol was more complex and not easily reversed. Thus HMG CoA reductase inhibitors reduced the ability of human lymphoblasts to expel an intracellular acid load via the Na(+)-H+ antiport, although the response of the antiport to an osmotic stimulus was preserved.

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