Mechanism of total glucosides from Chishao (Radix Paeoniae Rubra) on proliferation and apoptosis of hepatocellular carcinoma cells via phosphatase and tensin homolog deleted on chromosome ten / phosphatidylinositol 3-kinase / protein kinase B signaling pathway.

OBJECTIVE

To investigate the possible molecular mechanism of total glycosides of Chishao (Radix Paeoniae Rubra) (TG-RPR) on proliferation and apoptosis of hepatocellular carcinoma cells.

METHODS

The proliferation of TG-RPR on HepG2 cells was detected using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptosis of HepG2 cells was measured by annexin V-FITC/double staining. The phosphatase and tensin homolog deleted on chromosome ten (PTEN) / phosphatidylinositol 3-kinase (PI3K) / protein kinase B (Akt) signaling pathway was evaluated by Western Blot and reverse transcription-polymerase chain reaction (RT-PCR).

RESULTS

TG-RPR can up-regulation the expression of pro-apoptotic factors such as PTEN and BCL2-Associated X (Bax), down-regulation the expression of anti-apoptotic factors including B-cell lymphoma-2 (Bcl-2), PI3K, and Akt.

CONCLUSION

TG-RPR significantly inhibits the proliferation of HepG2 cells in a dose-dependent manner and promotes apoptosis. These results demonstrated TG-RPR has significant inhibitory effect on HepG2 cells. These results identify a critical role of TG-RPR in proliferation and apoptosis of HepG2 cells via modulating PTEN/PI3K/Akt signaling pathway. TG-RPR may offer a promise as a potential pharmaceutical therapy for hepatocellular carcinoma.