Biochemical and Biophysical Research Communications
Curcumin enhances the polyglutamine-expanded truncated N-terminal huntingtin-induced cell death by promoting proteasomal malfunction
Section snippets
Materials and methods
Materials. Curcumin, lactacystin, proteasome substrate, N-acetyl cysteine (NAC), rabbit polyclonal ubiquitin antibody, mouse monoclonal β-tubulin antibody, and all cell culture reagents were obtained from Sigma. LipofectAMINE 2000 and ponasterone A were obtained from Invitrogen, Mouse monoclonal anti-HA was obtained from Roche, and AP-conjugated anti-mouse and anti-rabbit IgG were from Vector Laboratories. Ubiquitin construct (with HA tag) was a kind gift from Dr. R. Takahashi, RIKEN Brain
Curcumin enhances the expanded polyglutamine protein-induced cell death
To test the possible effect of curcumin on the expanded polyglutamine protein-induced cell death we used stable and inducible cell lines that express truncated N-terminal huntingtin (tNhtt) fused with EGFP containing 16 and 150 glutamine residues. The cell lines were named HD 16Q and HD 150Q and their corresponding expressed proteins were named tNhtt-16Q and tNhtt-150Q. The cell lines were induced with 1 μM of ponasterone A for 2 days and then exposed to different doses of curcumin for 10 h. The
Discussion
Curcumin has long been used as a popular dietary spice and herbal medicine in several Southeastern countries. Different evidence suggests that curcumin has chemopreventive and anti-tumor activities because of its ability to induce apoptosis [19], [20], [21], [22]. The question was if there is any protective role of curcumin in Huntington’s disease and other polyglutamine diseases as were earlier shown in Alzheimer’s disease. The answer we got was not in affirmative. We found that curcumin
Acknowledgments
This work was supported by the Department of Biotechnology, Government of India. P.D. and A.M. were supported by research fellowship from Council of Scientific and Industrial Research, Government of India.
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