Constituents of ginger rhizome (Zingiber officinale Roscoe) inhibit Interleukin-1β maturation and secretion in stimulated human monocytes by a phospholipase A2 dependent manner

Ginger (Zingiber officinale Roscoe) is widely used against emesis and inflammatory diseases [1] but the exact mode of action remains to be elucidated. Functional inhibition of NF-κB and MAP kinases [2], or inhibition of COX-2 [3] were reported. The main constituent of ginger rhizome (6-gingerol) is believed to be the dominant active compound, but results on PGE2 inhibition [4] also indicates that several other chemically related compounds seem to be involved in the immunomodulatory effects.

We tested ginger extracts (50µg/ml) and pure compounds (10–50µM) in stimulated human whole blood and could show an inhibition of different cytokines in dependence of the used stimuli with the exception of interleukin-1β (IL-1β) being consequently down-regulated (up to 74% inhibition). Using Cytometric Bead Arrays and Western Blots we could demonstrate that in isolated human monocytes the iPLA₂ dependent maturation and the cPLA₂ dependent secretion are reduced, depending on assay conditions, to 3–22% and 61–88% respectively (at 10µg/ml), whereas transcription/translation was unaffected. Using flow cytometry we show that ion fluxes are not affected.

The suppression of secreted mature IL-1β as a key player in inflammatory diseases like rheumatism and the possible inhibition of phospholipases are likely to contribute to the anti-inflammatory potential of ginger preparations.

References: [1] Srivastava, K.C. et al. (1992) Med. Hypotheses 39:342–348.

[2] Kim, S.O. et al. (2004) Biofactors 21:27–31.

[3] Tjendraputra, E. et al. (2001) Bioorg. Chem. 29:156–163.

[4] Jolad, S.D. et al. (2004) Phytochemistry 65:1937–1954.