2009•Zhongguo aizheng zazhiRequires access
The regulatory effect of Curcumin on the differential expression of Bcl-2 and Caspase 8 and its promotional effect of apoptosis mechanism in human glioma cells
Zhixue Liu
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Abstract
Background and purpose:Neurospongioma is one of the most malignant brain tumors with a high mortality and poor prognosis, there are not many methods of prophylactic management for the disease. Curcumin, extracted from the bulbs of curcuma, belongs to Polyphenols. Previous research suggested that curcumin had the function of anti-oxygenation and anti-mutation. This study was done to investigate the regulatory effect of curcumin on the different expressions of Bcl-2 and Caspase 8 and its promotional effect of apoptosis mechanism in human glioma cells. Methods:Human glioma cell SHG44 was cultured in vitro. The growth inhibitory effect of curcumin on SHG44 cells was detected by MTT chromatometry. Cell cycles analysis was evaluated by flow cytometry(FCM). The morphological change and apoptosis alteration of SHG44 cells were identified by acridine orange(AO) staining. The differential expressions of Bcl-2 and Caspase 8 in SHG44 cells were examined by Western Blot. Results:Curcumin displayed a growth inhibitory effect on SHG44 cells in a dose-dependent manner[the IC50 of curcumin was (13.6±2.2) nmol/L,P0.01].The cell cycles analyses shown that cells were arrested at G0/G1 phases [curcumin group:(57.2±0.8)%;blank control:(64.6±0.6)%] and the proportion of sub-G0 cells was significantly increased in the cells treated with curcumin compared to the control group(25.9±0.2) (P0.01). The results of AO staining assay indicated that apparent apoptosis with occasional neorobiosis phenomena had taken place in the group treated with curcumin. Curcumin could increase the expression of Caspase 8[(96±23)%), P=0.001 3] and decrease the expression of Bcl-2[(33±8)%), P=0.001 4] at the curcumin dosage of IC50. Conclusion:Curcumin could not only regulate cell cycles of human glioma cells cultured in vitro, but also induce differential expressions of Bcl-2 and Caspase 8, and accelerate SHG44 cells to apoptosis.