Aims: Gallic acid (GA) is generally distributed in a variety of plants and foods, and possesses
cell growth-inhibiting activities in cancer cell lines. In the present study, the impact of GA on cell viability,
apoptosis induction and possible molecular mechanisms in cultured A549 lung carcinoma cells was investigated.
Methods:
In vitro experiments showed that treating A549 cells with various concentrations of GA inhibited cell
viability and induced apoptosis in a dose-dependent manner. In order to understand the mechanism by which
GA inhibits cell viability, comparative proteomic analysis was applied. The changed proteins were identified by
Western blot and siRNA methods.
Results:
Two-dimensional electrophoresis revealed changes that occurred to the cells when treated with or
without GA. Four up-regulated protein spots were clearly identified as malate dehydrogenase (MDH), voltagedependent,
anion-selective channel protein 1(VDAC1), calreticulin (CRT) and brain acid soluble protein
1(BASP1). VDAC1 in A549 cells was reconfirmed by western blot. Transfection with VDAC1 siRNA significantly
increased cell viability after the treatment of GA. Further investigation showed that GA down regulated
PI3K/Akt signaling pathways. These data strongly suggest that up-regulation of VDAC1 by GA may play an
important role in GA-induced, inhibitory effects on A549 cell viability.
Negative impacts of in-vitro oxidative stress on the quality of heat-induced myofibrillar protein gelation during refrigeration