| Summary: | 碩士 === 國立臺灣大學 === 毒理學研究所 === 81 === Apigenin, a plant flavonoid, could interfere TPA induced tumor
promoting phenomena in NIH3T3 cells, such as c-jun and c- fos
gene expression, 80kDa protein phosphorylation, lipid per-
oxidation and cell proliferation. In our study, TPA induced c-
fos gene expression in NIH3T3 cells suppressed by 10, 50, or
100mM of apigenin. On the other hand, TPA activated c-jun gene
expression also suppressed by apigenin. At 10mM of apigenin, c-
jun mRNA production repressed for 50%; at 100uM of apigenin,
TPA induced c-jun gene expression inhibited completely.
Apigenin could not interfere TPA binding to PKC, but could
inhibit TPA activated protein phosphorylation, and the
inhibition is time and doses dependent. Apigenin also repress
TPA induced lipid peroxidation in NIH3T3 cells. After TPA
treatment, cAMP concentration altered in a short time. At the
first hour, cAMP contains elevated 4.2 times, after that, TPA
induced cAMP elevation degraded. Apigenin also suppress TPA
induced cAMP elevation within 1 hour. Furthermore TPA induced
cell proliferation suppressed by apignin. From this result, we
suggest that apigenin suppresses TPA induced c-jun and c-fos
protooncogene expression, may through repress PKC and PKA
activation and free radical generation, lead to inhibited cell
proliferation that induced by TPA.
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