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

Abstract

PurposeTo 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.MethodsNeutrophils 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.ResultsNeutrophils 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.ConclusionAn 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.

In vitro anti-inflammatory activity of the Artemisia montana leaf ethanol extract in macrophage RAW 264.7 cells

“…The decrease in PGE 2 production was also observed with a methanol extract of a leaf mixture of A. argyi and A. princeps, an ethanol extract of A. asiatica Nakai, and a supercritical carbon dioxide extract of A. annua. These findings support the prevailing anti-inflammatory activity of Artemisia species, including A. montana, through the suppression of PGE 2 production (Hunt, Yoshida, Davis, Greenhill, & Davis, 2015;Jeong et al, 2014;Yun et al, 2016).…”

Phytochemical Analysis and Anti-Inflammatory Activity of Different Ethanolic Phyto-Extracts of Artemisia annua L.

“…Regarding the anti-inflammatory action, it has been observed that all AA derivatives inhibit the action of "mitogen-activated protein kinase" (MAPK), inhibit the transcription factor "nuclear factor kappa-B" (NF-κB), and inhibit the expression of the "Toll-Like Receptor" (TLR4 and TLR9) [11,12]. In addition, AA extracts in ethanol exhibit greater amounts of ART and exhibit a greater ability to block the inflammatory response induced by lipopolysaccharide (LPS) [13]. Furthermore, the phyto-extracts of AA were found to be effective in inhibiting the production of nitric oxide (NO), prostaglandins E2, and inflammatory cytokines (IL-1β and IL-6) in macrophage cultures under the pro-inflammatory stimulus elicited by LPS [13].…”

Artemisia annuaL. extracts inhibit thein vitroreplication of SARS-CoV-2 and two of its variants

“…Artemisinin delivered directly from the consumption of A. annua leaf powder is highly bioavailable and distributes through peripheral blood and into a plethora of organs including lungs, liver, heart, and brain (Desrosiers et al 2020). Furthermore, both artemisinins and the plant A. annua reduce levels of inflammatory cytokines including IL-6 and TNF-α in vivo (Desrosiers et al 2020; Hunt et al 2015; Shi et al 2015). These effector molecules can be problematic during the “cytokine storm” suffered by many SARS-CoV-2 patients (Schett et al 2020).…”