Milk Thistle (PDQ®)–Health Professional Version
SECTIONS
- Overview
- General Information
- History
- Laboratory/Animal/Preclinical Studies
- Human/Clinical Studies
- Adverse Effects
- Summary of the Evidence for Milk Thistle
- Changes to This Summary (06/19/2017)
- About This PDQ Summary
- View All Sections
Changes to This Summary (06/19/2017)
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
This summary was comprehensively reviewed.
Revised text to state that human clinical trials have investigated milk thistle or silymarin primarily in individuals with hepatitis or cirrhosis, although small studies have been reported about individuals with acute lymphoblastic leukemia, prostate cancer, breast cancer, head and neck cancer, and hepatocellular carcinoma; few adverse side effects have been reported for milk thistle, but little information about interactions with anticancer medications, radiation therapy, or other drugs is available.
Added text to state that in resistant glioma cell lines, silibinin was effective in potentiating the cytotoxic efficacy of temozolomide in LN229, U87, and A172 cells; silibinin also potentiated the effect of etoposide but not irinotecan in LN229 cells (cited Elhag et al. as reference 41).
Added text to state that the impact of silymarin and its components on signaling pathways have been investigated in several studies; in in vitro and in vivo studies utilizing the SK-MEL-5 melanoma cell line, silybin significantly inhibited growth through its direct binding with MEK1/2 and ribosomal S6 kinase-2, resulting in the inhibition of catalytic kinase activities (cited Lee et al. as reference 51). Also added text to state that silibinin suppresses colorectal cancer cell growth and progression possibly through its anti-inflammatory activity by interfering with nuclear factor-kappa B activation (cited Raina et al. as reference 52).
Added text to state that silibinin inhibits prostate cancer cell–induced osteoclastogenesis, suggesting that silibinin may be useful clinically for the treatment of bone metastases; silibinin targets prostate cancer cell–induced osteoclast differentiation and activity of murine macrophage cells (cited Kavitha et al. as reference 57).
The section was extensively revised.
This summary is written and maintained by the PDQ Integrative, Alternative, and Complementary Therapies Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® - NCI's Comprehensive Cancer Database pages.
No hay comentarios:
Publicar un comentario