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Elmann, A., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, Bet Dagan, Israel
Telerman, A., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, Bet Dagan, Israel
Erlank, H., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, 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., Raymond and Beverly Sackler Faculty of Exact Sciences, School of chemistry, Tel Aviv University, Ramat Aviv, Israel
Beit-Yannai, E., Clinical Biochemistry and Pharmacology Department, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheba, Israel
Achillolide A is a natural sesquiterpene lactone that we have previously shown can inhibit microglial activation. In this study we present evidence for its beneficial effects on astrocytes under oxidative stress, a situation relevant to neurodegenerative diseases and brain injuries. Viability of brain astrocytes (primary cultures) was determined by lactate dehydrogenase (LDH) activity, intracellular ROS levels were detected using 2′,7′-dichlorofluorescein diacetate, in vitro antioxidant activity was measured by differential pulse voltammetry, and protein phosphorylation was determined using specific ELISA kits. We have found that achillolide A prevented the H2O2-induced death of astrocytes, and attenuated the induced intracellular accumulation of reactive oxygen species (ROS). These activities could be attributed to the inhibition of the H2O2-induced phosphorylation of MAP/ERK kinase 1 (MEK1) and p44/42 mitogen-activated protein kinases (MAPK), and to the antioxidant activity of achillolide A, but not to H2O2 scavenging. This is the first study that demonstrates its protective effects on brain astrocytes, and its ability to interfere with MAPK activation. We propose that achillolide A deserves further evaluation for its potential to be developed as a drug for the prevention/treatment of neurodegenerative diseases and brain injuries where oxidative stress is part of the pathophysiology. © 2016 by the authors.
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Achillolide a protects astrocytes against oxidative stress by reducing intracellular reactive oxygen species and interfering with cell signaling
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Elmann, A., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, Bet Dagan, Israel
Telerman, A., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, Bet Dagan, Israel
Erlank, H., Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, 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., Raymond and Beverly Sackler Faculty of Exact Sciences, School of chemistry, Tel Aviv University, Ramat Aviv, Israel
Beit-Yannai, E., Clinical Biochemistry and Pharmacology Department, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheba, Israel
Achillolide a protects astrocytes against oxidative stress by reducing intracellular reactive oxygen species and interfering with cell signaling
Achillolide A is a natural sesquiterpene lactone that we have previously shown can inhibit microglial activation. In this study we present evidence for its beneficial effects on astrocytes under oxidative stress, a situation relevant to neurodegenerative diseases and brain injuries. Viability of brain astrocytes (primary cultures) was determined by lactate dehydrogenase (LDH) activity, intracellular ROS levels were detected using 2′,7′-dichlorofluorescein diacetate, in vitro antioxidant activity was measured by differential pulse voltammetry, and protein phosphorylation was determined using specific ELISA kits. We have found that achillolide A prevented the H2O2-induced death of astrocytes, and attenuated the induced intracellular accumulation of reactive oxygen species (ROS). These activities could be attributed to the inhibition of the H2O2-induced phosphorylation of MAP/ERK kinase 1 (MEK1) and p44/42 mitogen-activated protein kinases (MAPK), and to the antioxidant activity of achillolide A, but not to H2O2 scavenging. This is the first study that demonstrates its protective effects on brain astrocytes, and its ability to interfere with MAPK activation. We propose that achillolide A deserves further evaluation for its potential to be developed as a drug for the prevention/treatment of neurodegenerative diseases and brain injuries where oxidative stress is part of the pathophysiology. © 2016 by the authors.
Scientific Publication
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