Inhibitory effect of exogenous basic fibroblast growth factor on radiation-induced apoptosis in C17.2 neural stem cells*,*,☆

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Abstract

BACKGROUND:

It had been verified that injuries of neural stem cells after radiation were a possible mechanism of radiation-induced injuries of the brain (RIB). Basic fibroblast growth factor had been confirmed to have protective effect on RIB, but the mechanism was not clear.

OBJECTIVE:

To explore the inhibitory effect of basic fibroblast growth factor on radiation-induced apoptosis in C17.2 neural stem cells.

DESIGN, TIME AND SETTING:

The randomized controlled study was performed at the Lin Binxin Research Center of Second Affiliated Hospital of Sun Yat-sen University from November 2006 to June 2008.

MATERIALS:

C17.2 neural stem cell was constructed from the cerebellum progenitor cell of mouse after been immortalized.

METHODS:

C17.2 neural stem cell was radiated by accelerator linear (8 Gy) to establish the radiation model in vitro, and then incubated in a 96-well plate at 1×107/L. Different amounts of basic fibroblast growth factor (0, 25, 50, 100 μg/L) (0 μg/L served as control) were used in C17.2 neural stem cells (200 μL per well).

MAIN OUTCOME MEASURES:

Cell activity and survive curve were determined by MTT assay. Apoptotic rate was detected by flow cytometry.

RESULTS:

With the increase in basic fibroblast growth factor concentration, proliferation ratio of C17.2 neural stem cells was significantly increased (P < 0.01), in a dose-effect relationship. The effect was the most significant when the concentration of basic fibroblast growth factor was 100 μg/L, without cytotoxicity. Results of flow cytometry demonstrated that apoptotic rate of C17.2 neural stem cells in the control group was higher than in the 25, 50 μg/L basic fibroblast growth factor group (P < 0.01). There had significant differences in apoptotic ratio among 25, 50 and 100 μg/L basic fibroblast growth factor groups (P < 0.05-0.01).

CONCLUSION:

Exogenous basic fibroblast growth factor has obvious inhibitory effect on radiation-induced apoptosis in C17.2 neural stem cells.

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