Planta Med 2015; 81(03): 215-221
DOI: 10.1055/s-0034-1396204
Biological and Pharmacological Activity
Original Papers
Georg Thieme Verlag KG Stuttgart · New York

Downregulation of Microglial Activation by Achillolide A

Anat Elmann
1   Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, Bet Dagan, Israel
,
Alona Telerman
1   Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, Bet Dagan, Israel
,
Sharon Mordechay
1   Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, Bet Dagan, Israel
2   Faculty of Agriculture, Food and Environmental Quality Sciences of the Hebrew University of Jerusalem, Rehovot, Israel
,
Hilla Erlank
1   Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, Bet Dagan, Israel
2   Faculty of Agriculture, Food and Environmental Quality Sciences of the Hebrew University of Jerusalem, Rehovot, Israel
,
Miriam Rindner
1   Department of Food Quality and Safety, Volcani Center, Agricultural Research Organization, Bet Dagan, Israel
,
Yoel Kashman
3   School of Chemistry, Tel Aviv University, Ramat Aviv, Israel
,
Rivka Ofir
4   Dead Sea & Arava Science Center and Regenerative Medicine & Stem Cell Research Center, Ben-Gurion University of the Negev, Beer-Sheba, Israel
› Author Affiliations
Further Information

Publication History

received 06 March 2014
revised 03 December 2014

accepted 09 December 2014

Publication Date:
05 February 2015 (online)

Abstract

Chronic inflammation has been implicated in the pathogenesis of various neurodegenerative diseases. During the neuroinflammatory process, microglial cells release neurotoxic and proinflammatory mediators. In the present study, using activity-guided fractionation, we have purified an anti-inflammatory compound determined by spectroscopic methods to be a sesquiterpene lactone named achillolide A from Achillea fragrantissima (Forsk.) Sch. Bip. In primary cultures of lipopolysaccharide-activated microglial cells, achillolide A inhibited the lipopolysaccharide-induced levels of proinflammatory and toxic mediators including glutamate, nitric oxide, matrix metalloproteinase-9, cyclooxygenase-2, induced nitric oxide synthase, interleukin-1β, and tumor necrosis factor-α. Achillolide A also exhibited an antioxidant capacity, as was shown in a cell free system as well as by its ability to reduce intracellular reactive oxygen species levels in microglial cells. Thus, achillolide A might have therapeutic potential for treatment of neurodegenerative diseases and deserves further studies.

Supporting Information

 
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