Sodium butyrate activates the extrinsic and intrinsic apoptotic processes in murine cementoblasts.

BACKGROUND

: The metabolic by-product butyric acid of Gram-negative anaerobic bacteria can invoke pathological effects on periodontal cells resulting in inflammation and further destruction of periodontium. However, limited researches on the effects of butyric acid on cementoblasts were reported. Therefore, this study aimed to investigate the type of cell death in murine cementoblast (OCCM.30) caused by adding the different concentrations of sodium butyrate to the cell culture.

MATERIALS AND METHODS

OCCM.30 cells were exposed to sodium butyrate (0, 2, 4, 8, 16 mM) for 48 h. Cell viability was determined by microculture tetrazolium assay. Cell cycle distribution and cell death were analyzed by flow cytometry. Caspase-mediated apoptotic cascade was evaluated by Western blot.

RESULTS

The concentrations of sodium butyrate≧4 mM were found to inhibit cell viability of OCCM.30 cells in a dose-dependent manner ( < 0.05). Sodium butyrate elevated sub-G1 cell population which exhibited cell apoptosis in OCCM.30 cells ( < 0.05). In addition, early and later apoptotic cells were found in sodium butyrate-induced cell death. Sodium butyrate significantly stimulated the degradation of procaspases-3, -8, and -9 levels, respectively ( < 0.05). Simultaneously, sodium butyrate corresponded to augment the levels of cleaved forms of caspases-3, -8, and -9, respectively ( < 0.05).

CONCLUSION

Taken together, sodium butyrate is a cytotoxic agent and can induce apoptosis on cementoblasts. The pathway involved in apoptosis is activated by caspase family signaling pathways. These evidences may provide a new mechanistic insight into the mechanism of damage of cementoblasts during the development and progression of periodontitis.