This article review and discuss the complimentary and alternative medicine (CAM), where it all began, practices and ideas self- defined by their users as preventing and treating illnesses or promoting health and well-being.
HERB-DRUG INTERACTIONS ; HERBALS ; ECHINACEA ; TANACETUM PARTHENIUM ; GARLIC ; GINKGO BILOBA ; PANAX ; KAVA ; VALERIAN ; HYPERICUM ; EPHEDRA

Parthenolide (PTL) is a sesquiterpene lactone derived from medicinal plant feverfew (Tanacetum parthenium). Recent studies have demonstrated that it has multiple pharmacological activities, especially in the treatment of various hematological and solid cancers. The superior anticancer activity of PTL suggests that it has the potential to be a first-line drug. However, due to the limited physical and chemical properties, as well as bioavailability, structural modification strategies are strongly recommended to improve the anticancer activity. This review describes representative PTL derivatives obtained by different modification strategies, which are reported to exert antiproliferative activities superior to the parent compound PTL. Furthermore, we also summarize their basic mechanisms on cancer-related signaling pathways, so as to explain the potential and characteristics of PTL and its derivatives in cancer therapy.
Sesquiterpenes/chemistry* ; Tanacetum parthenium/metabolism* ; Antineoplastic Agents/pharmacology* ; Plant Extracts ; Neoplasms/drug therapy*

BACKGROUND/AIMS: Parthenolide (PT) is responsible for the bioactivities of Feverfew. Besides its potent anti-inflammatory effect, this compound has recently been reported to induce apoptosis in cancer cells. Unfortunately, many of the therapies that use 5-fluorouracil (5-FU) alone or in combination with other agents are likely to become ineffective due to drug resistance. In the present study, we investigate the antitumor effect of PT combined with 5-FU on colorectal cancer cells. METHODS: SW480 cell was employed as a representative of human colorectal carcinoma (CRC) cells. We performed MTT, annexin-V assay, and Hoechst 33258 staining to measure the synergistic effect. Western blotting was used to demonstrate apoptotic pathway. RESULTS: Our result demonstrated that PT inhibited the viability of colorectal cancer cells and had synergistic anti-proliferation in combination with 5-FU. After combined treatment of 5-FU and PT, enhanced apoptotic cell death is observed using annexin-V FITC assay and it was revealed by the condensed chromatin and fragmented DNA. Compared with 5-FU or PT alone, the apoptosis of colorectal cancer cells treated with PT and 5-FU enhanced the activation of caspase-8, caspase-3. CONCLUSIONS: Combined treatment with PT may offer an efficacious strategy to overcome 5-FU resistance in certain CRC cells.
Apoptosis ; Bisbenzimidazole ; Blotting, Western ; Caspase 8 ; Cell Death ; Chromatin ; Colorectal Neoplasms ; DNA ; Drug Resistance ; Fluorescein-5-isothiocyanate ; Fluorouracil ; Humans ; Sesquiterpenes ; Tanacetum parthenium

BACKGROUND/AIMS: Parthenolide (PT), a principle component derived from feverfew (Tanacetum parthenium), is a promising anticancer agent and has been shown to promote apoptotic cell death in various cancer cells. In this study, we focused on its functional role in apoptosis, migration, and invasion of human colorectal cancer (CRC) cells. METHODS: SW620 cells were employed as representative human CRC cells. We performed the MTT assay and cell cycle analysis to measure apoptotic cell death. The wound healing, Transwell migration, and Matrigel invasion assays were performed to investigate the effect of PT on cell migration/invasion. Western blotting was used to establish the signaling pathway of apoptosis and cell migration/invasion. RESULTS: PT exerts antiproliferative effect and induces apoptotic cell death of SW620 cells. In addition, PT prevents cell migration and invasion in a dose-dependent manner. Moreover, PT markedly suppressed migration/invasion-related protein expression, including E-cadherin, β-catenin, vimentin, Snail, cyclooxygenase-2, matrix metalloproteinase-2 (MMP-2), and MMP-9 in SW620 cells. PT also inhibited the expression of antiapoptotic proteins (Bcl-2 and Bcl-xL) and activated apoptosis terminal factor (caspase-3) in a dose-dependent manner. CONCLUSIONS: Our results suggest that PT is a potential novel therapeutic agent for aggressive CRC treatment.
Apoptosis ; Blotting, Western ; Cadherins ; Cell Cycle ; Cell Death* ; Cell Movement ; Colorectal Neoplasms ; Cyclooxygenase 2 ; Humans ; Matrix Metalloproteinase 2 ; Snails ; Tanacetum parthenium ; Vimentin ; Wound Healing