Curcuminoids, natural plant components, have been recently shown to display antioxidant and anti-inflammatory activities. They also produce potent chemo-preventive action against several types of cancer. In the present study, the anti-proliferative and induced apoptosis effects of curcuminoids have been investigated in human brain glioblastoma multiforme (GBM) 8401 cells. Results indicated that curcuminoids have produced an inhibition of cell proliferation in a dose-dependent manner as dosage increased from 12.5 to 100 μM (n = 6) via the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay as well as activation of apoptosis in GBM 8401 cells. Both effects were observed to increase in proportion with the dose of curcuminoids. We have studied the mitochondrial membrane potential (ΔΨm), DNA fragmentation, caspase-3, caspase-8, and caspase-9 activation, and nuclear factor κB (NF-κB) transcriptional factor activity to analyze apoptosis in GBM 8401 cells. From these approaches, apoptosis was induced by curcuminoids in human brain GBM 8401 cells via mitochondria and a caspase-dependent pathway. The results observed with proliferation inhibition (y = 94.694e(-0.025x), R(2) = 0.9901, and n = 6) and apoptosis (y = 0.9789e(-0.0102x), R(2) = 0.99854, and n = 3) depend upon the amount of curcuminoid treatment in the cancer cells.

Demethoxycurcumin (DMC; a curcumin-related demethoxy compound) has been recently shown to display antioxidant and antitumor activities. It has also produced a potent chemopreventive action against cancer. In the present study, the antiproliferation (using the MTT assay, DMC was found to have cytotoxic activities against GBM 8401 cell with IC50values at 22.71 μM) and induced apoptosis effects of DMC have been investigated in human brain malignant glioma GBM 8401 cells. We have studied the mitochondrial membrane potential (MMP), DNA fragmentation, caspase activation, and NF-κB transcriptional factor activity. By these approaches, our results indicated that DMC has produced an inhibition of cell proliferation as well as the activation of apoptosis in GBM 8401 cells. Both effects were observed to increase in proportion with the dosage of DMC treatment, and the apoptosis was induced by DMC in human brain malignant glioma GBM 8401 cells via mitochondria- and caspase-dependent pathways.

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