September 15, 2011

Feverfew, a member of the Asteraceae or Compositae family, is a perennial herb with a long history of traditional use.

The expression "feverfew" is derived from the Latin for fever reducer. Evidence of the anti-inflammatory properties of feverfew has been accruing over the last several decades and is now considered well established (Carcinogenesis 2004;25:1449-58).

Photo (c)Courtesy Wikimedia Commons/Dr Paul G Tuli/Creative Commons License   The feverfew extract parthenolide has anti-tumor and anti-inflammatory properties, but it has also been found to cause contact dermatitis and allergic reactions in some individuals.

In a Medline literature review of herbal agents that many people take but that might warrant discontinuing before dermatologic surgery, authors cited feverfew for its known success as a treatment for migraines (Br. Med. J. [Clin. Res. Ed.] 1985;291:569-73). In addition, feverfew is known for success in treatment for arthritis, as well as its anti-inflammatory activity in blocking phospholipase breakdown of arachidonic acid into prostaglandins and leukotrienes (Dermatol. Surg. 2001;27:759-63; Prostaglandins Leukot. Med. 1982;8:653-60).

They noted that platelet aggregation is also induced by the feverfew extract parthenolide and a byproduct of the arachidonic acid cascade, thromboxane A (Dermatol. Surg. 2001;27:759-63; J. Pharm. Pharmacol. 1990;42:553-7; J. Pharm. Pharmacol. 1987;39:459-65). Parthenolide is obtained as a hydroalcoholic extract of aerial parts of the plant, and is known to inhibit nuclear factor–kappaB (NF-kappaB) and to exhibit antiproliferative properties (Biochem. Biophys. Res. Commun. 2005;332:321-5). Feverfew also contains the potent antioxidant melatonin (Lancet 1997;350:1598-9).

Parthenolide Potency

Parthenolide has been consistently shown to exhibit in vitro antitumor activity (Mol. Cancer Ther. 2005;4:1004-12). A recent in vitro and in vivo investigation of the cancer chemopreventive potential of parthenolide using the UVB-induced skin cancer model revealed that SKH-1 hairless mice that were given parthenolide exhibited later onset of papillomas and significantly fewer papillomas in comparison to mice that were exposed only to UVB but not fed the primary component of feverfew. The in vitro phase of the study, which used cultured JB6 murine epidermal cells, showed that noncytotoxic concentrations of parthenolide pretreatment significantly suppressed UVB-induced activator protein-1 DNA binding and transcriptional activity, as well as JNK (c-Jun N-terminal kinase) and p38 MAP (mitogen-activated protein) kinase signaling activation, all of which might be crucial in the anticancer mechanism of action of parthenolide, according to the authors (Carcinogenesis 2004;25:1449-58). In a study conducted by three of the same investigators, parthenolide was found to sensitize UVB-induced apoptosis through pathways that depend on protein kinase C (Carcinogenesis 2005;26:2149-56).

In another recent study, investigators found that parthenolide effectively blocked the gene expression mediated by NF-kappaB and the production of bFGF (basic fibroblast growth factor) and MMP-1 (matrix metalloprotease-1) as well as the UVB-induced proliferation of keratinocytes and melanocytes in mouse skin, prompting the conclusion that inhibitors of NF-kappaB, particularly parthenolide, have potential to prevent cutaneous photoaging (J. Pharmacol. Exp. Ther. 2005;315:624-30).

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