Peroxyl radical scavenging activity of Ginkgo biloba extract EGb 761 (original) (raw)
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Effects of Gingko Extract (EGb761) on oxidative damage under different conditions of serum supply
Journal of Bioenergetics and Biomembranes, 2009
Standardized Ginkgo biloba extract EGb761 is known to have multivalent properties such as anti-oxidation and anti-apoptosis. In this study, we determined in rat pheochromocytoma (PC12) cells effects of EGb761 treatment on oxidative damage under three different conditions of serum supply: normal growth medium (NGM), serum deprivation (SE) and serum deprivation followed by resupply (SERS). It was found that, under the condition of serum deprivation, oxidative damage induced less cell death than the condition of serum supply. This appears to be related to inhibition of mitochondrial metabolism. Moreover, after serum deprivation, serum re-supply exacerbated cell necrosis, possibly through enhancement of oxidative damage. EGb761 could attenuate oxidative damage under the condition of serum supply whereas no protective effect on serum-depleted cells was observed. These results suggest that, there is a synergistic effect between trophic factors and EGb761. EGb761 treatment may protect cells from possible oxidative damage induced by the trophic factors. On the other hand, trophic factors appear to strengthen the protective effect of EGb761. To fully understand the synergistic interaction between antioxidants and trophic factors will help to sort out rational use of drugs in clinic practice.
PubMed, 2008
Dietary antioxidants are frequently proposed as protective agents for the vascular endothelium during the onset of atherosclerosis. This protection may occur at two distinct levels. First, they prevent oxidative modification of atherogenic lipoproteins (LDL). Second, they can provide a cellular protection against oxidized LDL-mediated endothelium dysfunction, although this mechanism remains poorly considered in many instances. To gain insight into the mechanism underlying such cellular protection against oxidized LDL, we examined the impact of a popular traditional medicine, an extract from Ginkgo biloba with well-known antioxidant properties, on two endothelial cells properties: cell adhesion and ionic homeostasis. Cellular lipoperoxides levels were also measured as a marker of cellular oxidative stress. Human umbilical-vein endothelial cells were exposed to native (nat-) or oxidized (ox-) LDL, the latter prepared to be compatible with clinically observed levels of oxidation. Although nat-LDL had little effect, ox-LDL increased endothelial adhesive properties (35%, p<0.01) and lipoperoxidation (45%, p<0.01). Na,K-ATPase activity, a key regulator of ionic homeostasis, was significantly decreased after exposure to nat-LDL (30%, p<0.01) and dramatically depressed after exposure to ox-LDL (65%, p<0.001). The standardized preparation of Ginkgo biloba EGb-761 totally protected adhesive properties and endothelial lipoperoxide levels. Moreover, it limited the decrease in Na,K-ATPase activity induced by ox-LDL to levels similar to nat-LDL. This suggests that EGb-761 protects endothelial adhesive properties and helps prevent the disruption of ionic homeostasis. The EGb-761-mediated inhibition of ox-LDL-induced lipoperoxide levels in endothelial cells appears to be an important mechanism by which Ginkgo biloba extract protects endothelial properties.
Prostaglandins Leukotrienes and Essential Fatty Acids, 2000
Ginkgo biloba extract (EGb 761) has beneficial effects on cognitive functions in aging patients, and on various pathologies, including cardiovascular diseases. Although the extract is known to have antioxidant properties and improve membrane fluidity, the cellular mechanisms underlying these effects have not been determined. Here, we examined the in vivo effects of EGb 761 on circulating and cellular lipids. EGb 761 treatment induced significant increases in the levels of circulating polyunsaturated fatty acids (PUFAs), and a decrease in the saturation index SI (saturated/polyunsaturated species). Plasma triglycerides and cholesterol were not affected, while phospholipids were slightly increased at the higher dose of EGb 761. EGb 761 treatment also induced a significant increase in the levels of PUFAs in erythrocyte membranes, especially for the eicosapentaenoic acid (EPAω3), and a decrease in the saturation index. Moreover, the response of erythrocytes to oxidative stress was improved in EGb 761-treated animals (H2O2-induced cell lysis decreased by 50%). Considering that PUFAs are known to improve membrane fluidity and response to oxidative damage, and are precursors of signaling molecules such as prostaglandins, the effects of EGb 761 on circulating and cellular PUFAs may explain some of the pharmacological properties of Ginkgo biloba.
Evaluating the In Vitro Potential of Natural Extracts to Protect Lipids from Oxidative Damage
Antioxidants
Lipid peroxidation is a chemical reaction known to have negative impacts on living organisms’ health and on consumer products’ quality and safety. Therefore, it has been the subject of extensive scientific research concerning the possibilities to reduce it, both in vivo and in nonliving organic matrices. It can be started by a variety of oxidants, by both ROS-dependent and -independent pathways, all of them reviewed in this document. Another feature of this reaction is the capacity of lipid peroxyl radicals to react with the non-oxidized lipids, propagating the reaction even in the absence of an external trigger. Due to these specificities of lipid peroxidation, regular antioxidant strategies—although being helpful in controlling oxidative triggers—are not tailored to tackle this challenge. Thus, more suited antioxidant compounds or technologies are required and sought after by researchers, either in the fields of medicine and physiology, or in product development and biotechnology....
The antioxidant activity of standardized extract ofGinkgo biloba (EGb 761) in rats
Phytotherapy Research, 2001
The standardized extract of Ginkgo biloba (EGb 761) has been widely employed for its significant benefit in neurodegenerative disorders. Although antioxidative actions have been attributed to this extract, the mechanisms of the multiple principles involved in this pharmacological activity are not completely established. Parkinson's and Alzheimer's diseases are frequently associated with oxidative stress and defects in the cellular protective mechanisms. In this study, the lipid peroxidation (LPO) and the activity of the antioxidant enzymes, catalase (CAT) and superoxide dismutase (SOD) were evaluated in the hippocampus, striatum and substantia nigra (SN) of rats treated with EGb 761. An increase in the CAT and SOD activities in the hippocampus, striatum and SN, and a decrease of the LPO in the hippocampus were observed. These data are additional to the antioxidant properties of EGb 761 reported in the literature and indicate a possible role for the extract in the treatment of diseases involving free radicals and oxidative damage.
Lipids, 2002
The antioxidant action on lipid peroxidation of the synthesized selenium compounds 1-(11-selenadodecyl)glycerol (SeG) and 1-(11-selenadodecyl)-3-Trolox-glycerol (SeTrG, where Trolox = 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid) was investigated. We compared the reactivity of the selenium compounds toward peroxyl radicals and their inhibitory effect on lipid peroxidation, induced by several kinds of initiating species such as azo compounds, metal ions, and superoxide/nitric oxide in solution, micelles, membranes, and rat plasma. SeTrG, but not SeG, scavenged peroxyl radicals. SeG reduced methyl linoleate hydroperoxides in organic solution and in methyl linoleate micelles oxidized by ferrous ion (Fe 2+ )/ascorbic acid. In rat plasma SeG and SeTrG decreased the formation of lipid hydroperoxides generated by hydrophilic azo compounds. SeG and SeTrG spared α-tocopherol (α-TOH) consumption in multilamellar vesicle membranes oxidized by hydrophilic or lipophilic initiators, and only SeTrG spared α-TOH in superoxide/nitric oxide oxidized membranes. In rat plasma oxidized by radical initiators (either hydrophilic or lipophilic) or superoxide/nitric oxide, SeTrG suppressed α-TOH consumption, but SeG had no effect. The two selenium-containing compounds showed inhibitory effects on lipid peroxidation that depended on their structure, the medium where they acted, and the oxidant used.
Reactive Oxygen Species, Lipid Peroxidation and Antioxidative Defense Mechanism
Lipid peroxidation can be defined as the oxidative deterioration of lipids containing any number of carbon-carbon double bonds. Lipid peroxidation is a well-established mechanism of cellular injury in both plants and animals, and is used as an indicator of oxidative stress in cells and tissues. Lipid peroxides are unstable and decompose to form a complex series of compounds including reactive carbonyl compounds. The oxidation of linoleates and cholesterol is discussed in some detail. Analytical methods for studying lipid peroxidation were mentioned. Various kinds of antioxidants with different functions inhibit lipid peroxidation and the deleterious effects caused by the lipid peroxidation products.
Pharmacological Applications of Antioxidants: Lights and Shadows
Current Drug Targets, 2014
Oxidative stress is linked with many pathologies ranging from cancer to neurodegenerative disorders and antioxidants have presumably therapeutic value in such diseases. In this review, we categorize different direct and indirect mechanisms by which antioxidants exert their action. These include scavenging and metal chelating effects, mimicking the antioxidant enzymes or upregulation of their expression, activation of nuclear factor erythroid 2-related factor 2 (Nrf2), increasing the activity of sirtuins and inhibition of pro-oxidant enzymes among others. Recent findings on the most frequently investigated antioxidants including polyphenolics, thiolics, spin trapping agents, SOD mimetics, inducers of heme oxygenase-1 and nitric oxide synthase, activators of Nrf2, NADPH oxidase inhibitors and herbal supplements are summarized. Furthermore, the antioxidant effects of drugs that are clinically used for other pharmacological purposes including ACE inhibitors and statins are discussed. Cost-effectiveness and adverse effects of antioxidants are also evaluated. Since antioxidant therapy has failed in many instances, we have classified the reasons that may explain these shortcomings in different categories. Novel approaches to antioxidant therapy, that include mitochondria-targeting drugs, antioxidant gene therapy and approaches for improvement of cell uptake and alteration of subcellular compartment localization are also described. In the end, "shadows" that are shortcomings of antioxidant therapy as well as "lights" that include positive outcomes are addressed. It is concluded that if we learn from failures, invest on agents with higher potential and take advantage of novel emerging approaches, antioxidants could be an asset for the management of certain carefully chosen oxidative stress-related diseases. vii. pulmonary diseases, including chronic obstructive pulmonary disease (COPD) [22] and asthma [23]; viii. chronic kidney disease (CKD) [24]; ix. psychiatric disorders, including depression [25], bipolar disorder [26] and schizophrenia [27].
Superoxide anion scavenging effect and superoxide dismutase activity of Ginkgo biloba extract
Experientia, 1989
Ginkgo biloba extract is known to be efficient in diseases associated with free radical generation. The purpose of this work was to study, under in vitro conditions, the action of Ginkgo biloba extract (Gbe) against superoxide anion (O2=), which is directly or indirectly implicated in cell damage. Gbe appears to have both an Oav scavenging effect and also a superoxide dismutase activity. Its antiradical effect was demonstrated by low temperature electron spin resonance and in a non-enzymatic system (phenazine methosulfate-NADH), and its enzymatic activity was shown by polarographic determination.