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פותח על ידי קלירמאש פתרונות בע"מ -
3,5,4′-Trihydroxy-6,7,3′-trimethoxyflavone protects astrocytes against oxidative stress via interference with cell signaling and by reducing the levels of intracellular reactive oxygen species
Year:
2014
Source of publication :
Neurochemistry International
Authors :
אלמן, ענת
;
.
ארלנק, הילה
;
.
טלרמן, אלונה
;
.
רינדנר, מרים
;
.
Volume :
78
Co-Authors:
Elmann, A., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, POB 6 Bet Dagan, Bet Dagan, Israel
Telerman, A., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, POB 6 Bet Dagan, Bet Dagan, Israel
Mordechay, S., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, POB 6 Bet Dagan, Bet Dagan, Israel
Erlank, H., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, POB 6 Bet Dagan, Bet Dagan, Israel
Rindner, M., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, POB 6 Bet Dagan, Bet Dagan, Israel
Ofir, R., Dead Sea and Arava Science Center, Regenerative Medicine and Stem Cell Research Center, Ben-Gurion University of the Negev, Beer-Sheba, Israel
Kashman, Y., School of Chemistry, Tel Aviv University, Ramat Aviv, Israel
Facilitators :
From page:
67
To page:
75
(
Total pages:
9
)
Abstract:
Oxidative stress is tightly involved in various neurodegenerative diseases such as Parkinson's and Alzheimer's diseases, and conditions such as ischemia. Astrocytes, the most abundant glial cells in the brain, protect neurons from reactive oxygen species (ROS) and provide them with trophic support. Therefore, any damage to astrocytes will affect neuronal survival. In a previous study we have demonstrated that an extract prepared from the plant Achillea fragrantissima (Af) prevented the oxidative stress-induced death of astrocytes and attenuated the intracellular accumulation of ROS in astrocytes under oxidative stress. In the present study, using activity guided fractionation, we have purified from this plant the active compound, determined to be a flavonoid named 3,5,4′-trihydroxy-6,7,3′-trimethoxyflavone (TTF). The effects of TTF in any biological system have not been studied previously, and this is the first study to characterize the anti-oxidant and protective effects of this compound in the context of neurodegenerative diseases. Using primary cultures of astrocytes we have found that TTF prevented the hydrogen peroxide (H2O2)-induced death of astrocytes, and attenuated the intracellular accumulation of ROS following treatment of these cells with H2O2 or the peroxyl radicals generating molecule 2,2′-Azobis(amidinopropane) (ABAP). TTF also interfered with cell signaling events and inhibited the phosphorylation of the signaling proteins stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), extracellular signal regulated kinase (ERK 1/2) and mitogen activated protein kinase kinase (MEK1) and the phosphorylation of the transcription factor cyclic AMP response element-binding protein (CREB). The mechanism of the protective effect of TTF against H2O2-cytotoxicity could not be attributed to a direct H2O2 scavenging but rather to the scavenging of free radicals as was shown in cell free systems. Thus, TTF might be a therapeutic candidate for the prevention/treatment of neurodegenerative diseases where oxidative stress is part of the pathophysiology. © 2014 Elsevier Ltd.
Note:
Related Files :
Achillea
Animals
flavonoids
Male
neurodegenerative diseases
reactive oxygen species
עוד תגיות
תוכן קשור
More details
DOI :
10.1016/j.neuint.2014.09.003
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
31041
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:59
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Scientific Publication
3,5,4′-Trihydroxy-6,7,3′-trimethoxyflavone protects astrocytes against oxidative stress via interference with cell signaling and by reducing the levels of intracellular reactive oxygen species
78
Elmann, A., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, POB 6 Bet Dagan, Bet Dagan, Israel
Telerman, A., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, POB 6 Bet Dagan, Bet Dagan, Israel
Mordechay, S., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, POB 6 Bet Dagan, Bet Dagan, Israel
Erlank, H., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, POB 6 Bet Dagan, Bet Dagan, Israel
Rindner, M., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, POB 6 Bet Dagan, Bet Dagan, Israel
Ofir, R., Dead Sea and Arava Science Center, Regenerative Medicine and Stem Cell Research Center, Ben-Gurion University of the Negev, Beer-Sheba, Israel
Kashman, Y., School of Chemistry, Tel Aviv University, Ramat Aviv, Israel
3,5,4′-Trihydroxy-6,7,3′-trimethoxyflavone protects astrocytes against oxidative stress via interference with cell signaling and by reducing the levels of intracellular reactive oxygen species
Oxidative stress is tightly involved in various neurodegenerative diseases such as Parkinson's and Alzheimer's diseases, and conditions such as ischemia. Astrocytes, the most abundant glial cells in the brain, protect neurons from reactive oxygen species (ROS) and provide them with trophic support. Therefore, any damage to astrocytes will affect neuronal survival. In a previous study we have demonstrated that an extract prepared from the plant Achillea fragrantissima (Af) prevented the oxidative stress-induced death of astrocytes and attenuated the intracellular accumulation of ROS in astrocytes under oxidative stress. In the present study, using activity guided fractionation, we have purified from this plant the active compound, determined to be a flavonoid named 3,5,4′-trihydroxy-6,7,3′-trimethoxyflavone (TTF). The effects of TTF in any biological system have not been studied previously, and this is the first study to characterize the anti-oxidant and protective effects of this compound in the context of neurodegenerative diseases. Using primary cultures of astrocytes we have found that TTF prevented the hydrogen peroxide (H2O2)-induced death of astrocytes, and attenuated the intracellular accumulation of ROS following treatment of these cells with H2O2 or the peroxyl radicals generating molecule 2,2′-Azobis(amidinopropane) (ABAP). TTF also interfered with cell signaling events and inhibited the phosphorylation of the signaling proteins stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), extracellular signal regulated kinase (ERK 1/2) and mitogen activated protein kinase kinase (MEK1) and the phosphorylation of the transcription factor cyclic AMP response element-binding protein (CREB). The mechanism of the protective effect of TTF against H2O2-cytotoxicity could not be attributed to a direct H2O2 scavenging but rather to the scavenging of free radicals as was shown in cell free systems. Thus, TTF might be a therapeutic candidate for the prevention/treatment of neurodegenerative diseases where oxidative stress is part of the pathophysiology. © 2014 Elsevier Ltd.
Scientific Publication
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