The present invention provides a method of inhibiting the activation of the NF.kappa.B transcription factor in an animal in need of such treatment comprising the step of administering to said animal a pharmacologically effective dose of curcumin. Also provided is a method of inhibiting the nuclear translocation of the p65 subunit of the NF.kappa.B transcription factor in a cell or in an animal in need of such treatment comprising the step of administering to said animal a pharmacologically effective dose of curcumin.
Each gene in a group comprising many genes is cloned into an expression vector so that its gene product should be expressed as a fusion protein with a protein emitting self-fluorescence to construct a gene expression library. The gene expression library is introduced into cells of two groups to express the fusion proteins in the cells, and only one cell group is stimulated by a drug or the like. Then, cells in which the fusion proteins are localized in the nuclei or their nuclei are isolated from cells of the two groups, respectively. By comparing these cells, genes coding for proteins that are transported into the nuclei specifically in response to a certain stimulus when the stimulus is applied to the cells are retrieved.
The invention features a method for the treatment or prevention of mucositis in an individual undergoing or preparing to undergo cancer treatment. The method includes administering a therapeutically effective amount of an inhibitor of NF-.kappa.B to an individual undergoing or preparing to undergo a treatment for cancer. In certain embodiments, the inhibitor is a compound having the formula: ##STR1## where R.sub.1 and R.sub.4 are OH, and R.sub.2 and R.sub.3 are independently OH or H, provided that when R.sub.1 and R.sub.2 are both OH, R.sub.1 and R.sub.2 cannot be disposed ortho to one another, and when R.sub.3 and R.sub.4 are both OH, R.sub.3 and R.sub.4 cannot be disposed ortho to one another. The compounds of formula I may be cis or trans.
All multiple myeloma cell lines examined showed constitutively active I.kappa.B kinase (IKK), I.kappa.B.alpha. phosphorylation and constitutively active NF-.kappa.B. Curcumin, a chemopreventive agent, suppressed constitutive I.kappa.B.alpha. phosphorylation through inhibition of IKK activity and downregulated NF-.kappa.B. Curcumin also downregulated expression of NF-.kappa.B-regulated gene products such as I.kappa.B.alpha., Bcl-2, Bcl-x.sub.L, cyclin D1 and interleukin-6. Consequently, curcumin suppressed multiple myeloma cell proliferation and arrested cells at the G1/S phase of the cell cycle. Curcumin also induced apoptosis and chemosensitivity to vincristine. Overall, results presented herein provide a molecular basis for the treatment of multiple myeloma patients with this pharmacologically safe agent.
The present invention provides methods of inhibiting metastasis of a tumor and methods of treating a tumor using a combination of an inhibitor of the activation of nuclear factor NF-.kappa.B and a cancer chemotherapeutic agent. In one embodiment of the present invention, combination of curcumin and paclitaxel (taxol) can be used to treat and inhibit metastasis of breast tumor.
New pharmacological activities of Curcuma Longa extracts as antiproliferative and photosensitivisation agents and their use in proliferative diseases such as psoriasis, as reducers of plasmatic fibrinogen and the Apolipoprotein B/Apolipoprotein A-I quotient, without altering other coagulation parameters.
