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. 2015 Sep 2:15:301.
doi: 10.1186/s12906-015-0836-8.

Anticancer and apoptotic effects on cell proliferation of diosgenin isolated from Costus speciosus (Koen.) Sm

Affiliations

Anticancer and apoptotic effects on cell proliferation of diosgenin isolated from Costus speciosus (Koen.) Sm

Samy Selim et al. BMC Complement Altern Med. .

Abstract

Background: Diosgenin, a naturally occurring steroid saponin found abundantly in C. speciosus, is a well-known precursor of various synthetic steroidal drugs that are extensively used in the pharmaceutical industry.

Methods: The present study was conducted to evaluate the in vitro anticancer and apoptotic effects on cell proliferation of diosgenin isolated from C. speciosus (Koen.) Sm.

Results: The results indicated that the treatment of HepG2 cells with the sample resulted in a cytotoxic effect as concluded from the IC50 value 32.62 μg/ml, while the treatment of HepG2 cells with paclitaxel, a known anti-cancer drug, resulted in an IC50 value of 0.48 μg/ml. The treatment of MCF-7 cells with the tested sample resulted in high inhibition in the cell viability, and resulted in an IC50 value of 11.03 μg/ml, while the treatment of MCF-7 cells with paclitaxel resulted in an IC50 value of 0.61 μg/ml. The levels of DR4 and caspase-3 were significantly increased (P<0.01) in MCF-7 cells treated with the tested sample compared to untreated cells and possessed a similar activity of paclitaxel in DR4 induction but lower induction in caspase-3. On the other hand the treatment of macrophages or lymphocytes with diosgenin (250 μg/ml) resulted in an induction in the cell proliferation up to 3.2-fold and 2.1-fold of control, respectively.

Conclusions: The results presented here may suggest that diosgenin isolated from C. speciosus possess anticancer and apoptotic effects on cell proliferation, and therefore, can be used as pharmaceuticals drugs.

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Figures

Fig. 1
Fig. 1
Chemical structure of diosgenin
Fig. 2
Fig. 2
The cytotoxicity (% of control) of different concentrations (μg/ml) of the tested sample against (a) human HepG2, (b) human HL-60 and (c) human MCF-7 cells after 24 h of incubation as assayed by MTT. (n = 4)
Fig. 3
Fig. 3
Cell cycle analysis of MCF-7 cells: DNA frequency distribution of cells cultured in control (left), Sample-treated (right), in one representative capture
Fig. 4
Fig. 4
Representative images for the mode of cell death in the sample-treated MCF-7 cells (50 % of IC50), as stained by AO/EB and captured under fluorescence microscope (x200). Vital cells (green), early apoptotic (bright green to yellow), late apoptotic (orange) and necrotic cells (red)
Fig. 5
Fig. 5
The cell population percentage of vital (white segments), apoptotic (black segment) and necrotic (gray segments) cells were counted after treatment with the tested sample and paclitaxel. Results represent the mean of three independent experiments
Fig. 6
Fig. 6
The effect of treatment with the tested sample (black bars, 50 % of IC50) on apoptotic cell death pathway in MCF-7 cells compared with paclitaxel activity (gray bars). DR4 and caspase-3 levels in treated cells were compared with control cells. The data represented as number of folds in relation to control absorbance readings, which were 7.3, and 6.5 milliabsorbance, respectively
Fig. 7
Fig. 7
The proliferation (% of control) of different concentrations (μg/ml) of the tested sample in lymphoblastic leukemia 1301 cells (grey line) and Raw murine macrophage RAW 264.7 (black line) after 72 h of incubation as assayed by MTT. (n = 4)

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