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An extract of the medicinal plant Artemisia annua modulates production of inflammatory markers in activated neutrophils

Authors Hunt S, Yoshida M, Davis C, Greenhill N, Davis P

Received 7 October 2014

Accepted for publication 14 November 2014

Published 14 January 2015 Volume 2015:8 Pages 9—14

DOI https://doi.org/10.2147/JIR.S75484

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr Ning Quan


Sheena Hunt,1 Mayumi Yoshida,2 Catherine EJ Davis,2 Nicholas S Greenhill,2 Paul F Davis2

1Promisia Integrative Ltd, Wellington, New Zealand; 2Trinity Bioactives Ltd, Wellington, New Zealand

Purpose: To investigate the ability of a commercial extract from the medicinal plant Artemisia annua to modulate production of the cytokine, tumor necrosis factor-alpha (TNF-α), and the cyclooxygenase (COX) inflammatory marker, prostaglandin E2 (PGE2) in activated neutrophils.
Methods: Neutrophils were harvested from rat whole blood and cultured in the presence of plant extract or control samples. Neutrophils, except unactivated control cells, were activated with 10 µg/mL lipopolysaccharide (LPS). The cells were cultured with a range of different concentrations of the A. annua extracts (400–1 µg/mL) and artemisinin (200 and 100 µg/mL) and the supernatants were then tested by enzyme-linked immunosorbent assay (ELISA) for the concentrations of TNF-α and PGE2. Each sample was assayed in triplicate. Positive controls with an inhibitor were assayed in triplicate: chloroquine 2.58 and 5.16 µg/mL for TNF-α, and ibuprofen 400 µg/mL for PGE2. An unsupplemented group was also assessed in triplicate as a baseline control.
Results: Neutrophils were stimulated to an inflammatory state by the addition of LPS. A. annua extract significantly inhibited TNF-α production by activated neutrophils in a dose-dependent manner. There was complete inhibition by the A. annua extract at 200, 100, and 50 µg/mL (all P≤0.0003). At A. annua extract concentrations of 25, 10, and 5 µg/mL, TNF-α production was inhibited by 89% (P<0.0001), 54% (P=0.0002), and 38% (P=0.0014), respectively. A. annua 1 µg/mL did not significantly inhibit TNF-α production (8.8%; P>0.05). Concentrations of 400, 200, and 100 µg/mL A. annua extract significantly inhibited PGE2 production by 87% (P=0.0128), 91% (P=0.0017), and 93% (P=0.0114), respectively.
Conclusion: An extract of A. annua was shown to be a potent inhibitor of TNF-α and a strong inhibitor of PGE2 production in activated neutrophils at the concentrations tested. Further studies are warranted with this promising plant extract.

Keywords: in vitro, TNF-α, COX-2, PGE2, artemisinin, Arthrem

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