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Extracts of feverfew inhibit mitogen‐induced human peripheral blood mononuclear cell proliferation and cytokine mediated responses: a cytotoxic effect.
Author(s) -
O'Neill LA,
Barrett ML,
Lewis GP
Publication year - 1987
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1987.tb03012.x
Subject(s) - peripheral blood mononuclear cell , cytotoxic t cell , lymphokine , cytotoxicity , pharmacology , cytokine , parthenolide , immunology , chemistry , medicine , immune system , biochemistry , in vitro , apoptosis
Feverfew has been used since antiquity to treat inflammatory conditions. Extracts of the herb were found to inhibit mitogen‐induced tritiated thymidine ([3H]‐TdR) uptake by human peripheral blood mononuclear cells (PBMC), interleukin 2 (IL‐2)‐induced [3H]‐TdR uptake by lymphoblasts and PGE2 release by interleukin 1 (IL‐1)‐stimulated synovial cells. Parthenolide, a major secondary metabolite from the herb also blocked [3H]‐TdR uptake by mitogen‐induced PBMC. However, both crude extracts and parthenolide proved cytotoxic to mitogen‐ induced PBMC and IL‐1 stimulated synovial cells, the cytotoxic effect being functionally indistinguishable from the inhibitory effects. The pharmacological properties of feverfew may thus be due to cytotoxicity, although the time course of the events described in this paper is different from those where feverfew appears to have more specific inhibitory effects.