Gallic acid caused cultured mice TM4 Sertoli cells apoptosis and necrosis.
Paraules clau
Resum
UNASSIGNED
The study was designed to determine the cytotoxic effect of gallic acid (GA), obtained by the hydrolysis of tannins, on mice TM4 Sertoli cells apoptosis.
UNASSIGNED
In the present study, non-tumorigenic mice TM4 Sertoli cells were treated with different concentrations of GA for 24 h. After treatment, cell viability was evaluated using WST-1, mitochondrial dysfunction, cells apoptosis and necrosis was detected using JC-1, Hoechst 33342 and propidium iodide staining. The expression levels of Cyclin B1, proliferating cell nuclear antigen (PCNA), Bcl-2-associated X protein (BAX) and Caspase-3 were also detected by RT-PCR and Western-blotting.
UNASSIGNED
The results showed that 20-400 μM GA inhibited viability of TM4 Sertoli cells in a dose-dependent manner. Treatment with 400 μM GA significantly inhibited PCNA and Cyclin B1 expression, however up-regulated BAX and Caspase-3 expression, caused mitochondrial membrane depolarization, activated Caspase-3, and induced DNA damage, thus, markedly increased the numbers of dead cells.
UNASSIGNED
Our findings showed that GA could disrupt mitochondrial function and caused TM4 cells to undergo apoptosis and necrosis.
