Fig 1.
Fsitein inhibits growth of HepG-2, Caco-2 and Suit-2 cells.
Exponentially growing cells were cultured and treated with fisetin for 2 days. The SRB assay was then performed to assess cell viability and proliferation. Results are represented as mean value (M) ± S.E.M. of at least 3 independent experiments (8 replica each).
Fig 2.
Apoptotic effect of fisetin as shown by measuring caspase 3/7 activatioin.
Cells were treated with gradient concentrations of fisetin and caspase 3/7 assay was carried out. Results are presented as mean value (M) ± S.E.M. of at least 3 independent experiments (4 replica each), * significantly different from control group (P< 0.001) using 2 way ANOVA test.
Fig 3.
Inhibition of prostaglandin E2 after fisetin treatment of Caco-2 cells.
Results are represented as mean value (M) ± S.E.M of at least three independent experiments (4 replica each). * Significantly different from control group (P< 0. 05) using one way ANOVA test.
Fig 4.
Top 40 common biomarker genes expressed in both Suit-2 (A) and HepG-2 (B) cells. Arranged in a descending order according to gene expression levels in Suit-2 (I) and HepG-2 (II), respectively.
Table 1.
Confirmation of microarray gene expression results with Rt-PCR.
Fig 5.
Cell cycle: G2/M DNA damage checkpoint regulation after treating HepG-2 cells with fisetin.
Fig 6.
CDK5 signaling pathway after treating Suit-2 cells with fisetin.
Fig 7.
Effect of fisetin on CYP3A4 enzyme activity.
Fisetin inhibits CYP3A4 activity in a dose dependent manner. Results are presented as mean value (M) ± S.E.M. of at least 3 independent experiments (6 replica each).
Fig 8.
Effect of fisetin on GST enzyme activity.
Fisetin inhibits GST activity in a dose dependent manner. Results are presented as mean value (M) ± S.E.M. of at least 3 independent experiments (6 replicas each).