Protective effect of ginkgo biloba against gossypol-induced apoptosis in human lymphocytes (original) (raw)
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European Journal of Neuroscience, 2000
Substantial evidence suggests that the accumulation of b-amyloid (Ab)-derived peptides, and to a lesser extent free radicals, may contribute to the aetiology and/or progression of Alzheimer's disease (AD). Ginkgo biloba extract (EGb 761) is a well-de®ned plant extract containing two major groups of constituents, i.e.¯avonoids and terpenoids. It is viewed as a polyvalent agent with a possible therapeutic use in the treatment of neurodegenerative diseases of multifactorial origin, e.g. AD. We have investigated here the potential effectiveness of EGb 761 against toxicity induced by (Ab)-derived peptides (Ab 25±35 ,A b 1±40 and Ab 1±42 ) on hippocampal primary cultured cells, this area being severely affected in AD. A co-treatment with EGb 761 concentration-dependently (10±100 mg/ mL) protected hippocampal neurons against toxicity induced by Ab fragments, with a maximal and complete protection at the highest concentration tested. Similar, albeit less potent protective effects were seen with the¯avonoid fraction of the extract (CP 205), while the terpenes were ineffective. Most interestingly, EGb 761 (100 mg/mL) was even able to protect (up to 8 h) hippocampal cells from a pre-exposure to Ab 25±35 and Ab 1±40 . EGb 761 was also able to both protect and rescue hippocampal cells from toxicity induced by H 2 O 2 (50±150 mM), a major peroxide possibly involved in mediating Ab toxicity. Moreover, EGb 761 (10±100 mg/mL), and to a lesser extent CP 205 (10±50 mg/mL), completely blocked Ab-induced events, e.g. reactive oxygen species accumulation and apoptosis. These results suggest that the neuroprotective effects of EGb 761 are partly associated with its antioxidant properties and highlight its possible effectiveness in neurodegenerative diseases, e.g. AD via the inhibition of Ab-induced toxicity and cell death.
European Journal of Neuroscience, 2000
Substantial evidence suggests that the accumulation of b-amyloid (Ab)-derived peptides, and to a lesser extent free radicals, may contribute to the aetiology and/or progression of Alzheimer's disease (AD). Ginkgo biloba extract (EGb 761) is a well-de®ned plant extract containing two major groups of constituents, i.e.¯avonoids and terpenoids. It is viewed as a polyvalent agent with a possible therapeutic use in the treatment of neurodegenerative diseases of multifactorial origin, e.g. AD. We have investigated here the potential effectiveness of EGb 761 against toxicity induced by (Ab)-derived peptides (Ab 25±35 , Ab 1±40 and Ab 1±42) on hippocampal primary cultured cells, this area being severely affected in AD. A co-treatment with EGb 761 concentration-dependently (10±100 mg/ mL) protected hippocampal neurons against toxicity induced by Ab fragments, with a maximal and complete protection at the highest concentration tested. Similar, albeit less potent protective effects were seen with the¯avonoid fraction of the extract (CP 205), while the terpenes were ineffective. Most interestingly, EGb 761 (100 mg/mL) was even able to protect (up to 8 h) hippocampal cells from a pre-exposure to Ab 25±35 and Ab 1±40. EGb 761 was also able to both protect and rescue hippocampal cells from toxicity induced by H 2 O 2 (50±150 mM), a major peroxide possibly involved in mediating Ab toxicity. Moreover, EGb 761 (10±100 mg/mL), and to a lesser extent CP 205 (10±50 mg/mL), completely blocked Ab-induced events, e.g. reactive oxygen species accumulation and apoptosis. These results suggest that the neuroprotective effects of EGb 761 are partly associated with its antioxidant properties and highlight its possible effectiveness in neurodegenerative diseases, e.g. AD via the inhibition of Ab-induced toxicity and cell death.
Antioxidants, 2020
Oxidative stress has been associated to neuronal cell loss in neurodegenerative diseases. Neurons are post-mitotic cells that are very sensitive to oxidative stress—especially considering their limited capacity to be replaced. Therefore, reduction of oxidative stress, and inhibiting apoptosis, will potentially prevent neurodegeneration. In this study, we investigated the neuroprotective effect of Ginkgo biloba extract (EGb 761) against H2O2 induced apoptosis in SK-N-BE neuroblastoma cells. We analysed the molecular signalling pathway involved in the apoptotic cell death. H2O2 induced an increased acetylation of p53 lysine 382, a reduction in mitochondrial membrane potential, an increased BAX/Bcl-2 ratio and consequently increased Poly (ADP-ribose) polymerase (PARP) cleavage. All these effects were blocked by EGb 761 treatment. Thus, EGb 761, acting as intracellular antioxidant, protects neuroblastoma cells against activation of p53 mediated pathway and intrinsic mitochondrial apopto...
The effect of Ginkgo biloba extract on scopolamine-induced apoptosis in the hippocampus of rats
Anatomical Science International, 2013
Apoptosis, known as programmed cell death, plays a crucial role in normal development and tissue homeostasis. Apoptosis is also involved in neurodegenerative diseases such as Alzheimer's disease. Amnesia refers to the loss of memory and can also be a warning sign of neurodegenerative diseases. The antioxidant properties of Ginkgo biloba extract was known previously. Therefore, the aim of this study was to examine the effects of Ginkgo biloba extract on the rat's hippocampal apoptotic neurons number after Scopolamine based amnesia. Thirty-six adult male Wistar rats were used. Rats were randomly divided into control, sham, protective and treatment groups. The rats in the sham group received only scopolamine hydrobromide (3 mg/kg) intraperitoneally. The rats in the protective and treatment groups received Ginkgo biloba extract (40, 80 mg/kg) for 7 days intraperitoneally before/ after scopolamine injection. Then 48 h after the last injection, the brains of rats were withdrawn and fixed with paraformaldehyde, and then, after histological processing, the slices were stained with the TUNEL kit for apoptotic neurons. Data were compared by the ANOVA Post Hoc Tukey test; P \ 0.05 was considered significant. Our results showed that Scopolamine (in the sham group) increased significantly the number of apoptotic neurons in all areas of the hippocampus compared with the control. Whereas, Ginkgo biloba extract reduce the neuronal apoptosis in the hippocampus before and/or after encounter with scopolamine. We concluded that pretreatment and treatment injection of Ginkgo biloba extract can have a protective effect for neurons and it can limit apoptosis in all area of the hippocampus.
Ginkgo bilobaL.: Phytochemical components and antioxidant activity
African Journal of Pharmacy and Pharmacology, 2015
Curative effects of Ginkgo biloba L. have been recognized for centuries, dating back to traditional Chinese medicine which used crushed leaves to treat several health problems. Although G. biloba L. has several known and investigated activities, the antioxidant activity of its extract (EGb 761) is particularly relevant because reactive oxygen (ROS) and reactive nitrogen (RNS) species are constantly produced in aerobic organisms. Currently, the exploitation of the antioxidant activity of G. biloba extract Egb 761 has been of particular pharmacological importance because oxidative stress may be harmful to cells and may trigger the development of many disorders. The antioxidant activity of the EGb extract against oxidative stress has been associated with several therapeutic effects and currently, Egb761 is indicated to treat labyrinthitis, headache, memory disturbance, intermittent claudication, dementia, Alzheimer's disease, glaucoma, cardiovascular disorders, cerebral ischemia, increased libido and sexual activity, and psychiatric diseases, such as depression. This study is a review of basic and clinical studies related to antioxidant properties of G. biloba L.
Inhibition of amyloid- aggregation and caspase-3 activation by the Ginkgo biloba extract EGb761
Proceedings of the National Academy of Sciences, 2002
Standardized extract from the leaves of the Ginkgo biloba tree, labeled EGb761, has been used in clinical trials for its beneficial effects on brain functions, particularly in connection with agerelated dementias and Alzheimer's disease (AD). Substantial experimental evidence indicates that EGb761 protects against neuronal damage from a variety of insults, but its cellular and molecular mechanisms remain unknown. Using a neuroblastoma cell line stably expressing an AD-associated double mutation, we report that EGb761 inhibits formation of amyloid- (A) fibrils, which are the diagnostic, and possibly causative, feature of AD.
Ginkgo biloba extract in Alzheimer's disease: from action mechanisms to medical practice
International journal of molecular sciences, 2010
Standardized extract from the leaves of the Ginkgo biloba tree, labeled EGb761, is one of the most popular herbal supplements. Numerous preclinical studies have shown the neuroprotective effects of EGb761 and support the notion that it may be effective in the treatment and prevention of neurodegenerative disorders such as Alzheimer's disease (AD). Despite the preclinical promise, the clinical efficacy of this drug remains elusive. In this review, possible mechanisms underlying neuroprotective actions of EGb761 are described in detail, together with a brief discussion of the problem of studying this herb clinically to verify its efficacy in the treatment and prevention of AD. Moreover, various parameters e.g., the dosage and the permeability of the blood brain barrier (BBB), impacting the outcome of the clinical effectiveness of the extract are also discussed. Overall, the findings summarized in this review suggest that, a better understanding of the neuroprotective mechanisms of...
Inhibition of amyloid-β aggregation and caspase-3 activation by the Ginkgo biloba extract EGb761
Proceedings of the National Academy of Sciences, 2002
Standardized extract from the leaves of the Ginkgo biloba tree, labeled EGb761, has been used in clinical trials for its beneficial effects on brain functions, particularly in connection with age-related dementias and Alzheimer's disease (AD). Substantial experimental evidence indicates that EGb761 protects against neuronal damage from a variety of insults, but its cellular and molecular mechanisms remain unknown. Using a neuroblastoma cell line stably expressing an AD-associated double mutation, we report that EGb761 inhibits formation of amyloid-β (Aβ) fibrils, which are the diagnostic, and possibly causative, feature of AD. The decreased Aβ fibrillogenesis in the presence of EGb761 was observed both in the conditioned medium of this Aβ-secreting cell line and in solution in vitro . In the cells, EGb761 significantly attenuated mitochondrion-initiated apoptosis and decreased the activity of caspase 3, a key enzyme in the apoptosis cell-signaling cascade. These results suggest ...
Alzheimer's disease (AD) is the most common progressive human neurodegenerative disorder affecting elderly population worldwide. Hence, prevention of AD has been a priority of AD research worldwide. Based on understanding of disease mechanism, different therapeutic strategies involving synthetic and herbal approaches are being used against AD. Among the herbal extract, Ginkgo biloba extract (GBE) is one of the most investigated herbal remedy for cognitive disorders and Alzheimer's disease (AD). Standardized extract of Ginkgo biloba is a popular dietary supplement taken by the elderly population to improve memory and age-related loss of cognitive function. Nevertheless, its efficacy in the prevention and treatment of dementia remains controversial. Specifically, the added effects of GBE in subjects already receiving "conventional" anti-dementia treatments have been to date very scarcely investigated. This review summarizes recent advancements in our understanding of the potential use of Ginkgo biloba extract in the prevention of AD including its antioxidant property. A better understanding of the mechanisms of action of GBE against AD will be important for designing therapeutic strategies, for basic understanding of the underlying neurodegenerative processes, and for a better understanding of the effectiveness and complexity of this herbal medicine.
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.