Desipramine antagonized corticosterone-induced apoptosis in cultured PC12 cells.
Abstract
AIM: To study possible action mechanism of a tricyclic antidepressant,
desipramine (DIM).
METHODS: Cultured PC12 cells were exposed to corticosterone in the absence or
presence of DIM for 5 d. Agarose gel electrophoresis, flow cytometry, and
electron microscopy were used to detect the apoptosis of PC12 cells.
RESULTS: Corticosterone 10 micromol/L treatment for 5 d elicited typical
apoptotic biochemical and morphological changes including condensed chromatin
shaped like crescent moon, nuclear fragmentation, and DNA degradation. The
highest percentage of apoptotic cells accumulated to 28 % +/- 9 %. Agarose gel
electrophoresis showed typical DNA ladders pattern. While in the presence of DIM
1 or 5 micromol/L, apoptosis percentage was markedly decreased with lightened DNA
ladder and ultrastructure of the cells was improved.
CONCLUSION: DIM could antagonize the apoptosis in PC12 cells induced by
corticosterone, which may be one of the cellular mechanisms of its antidepressant
effect.
Keywords:
desipramine (DIM).
METHODS: Cultured PC12 cells were exposed to corticosterone in the absence or
presence of DIM for 5 d. Agarose gel electrophoresis, flow cytometry, and
electron microscopy were used to detect the apoptosis of PC12 cells.
RESULTS: Corticosterone 10 micromol/L treatment for 5 d elicited typical
apoptotic biochemical and morphological changes including condensed chromatin
shaped like crescent moon, nuclear fragmentation, and DNA degradation. The
highest percentage of apoptotic cells accumulated to 28 % +/- 9 %. Agarose gel
electrophoresis showed typical DNA ladders pattern. While in the presence of DIM
1 or 5 micromol/L, apoptosis percentage was markedly decreased with lightened DNA
ladder and ultrastructure of the cells was improved.
CONCLUSION: DIM could antagonize the apoptosis in PC12 cells induced by
corticosterone, which may be one of the cellular mechanisms of its antidepressant
effect.