Ginsenoside CK Induces the Mitochondrial Apoptosis in Glioma Cells Through the Activation of the p53-Bax-Caspase Pathway

Abstract

Background: Gliomas are harmful to human health; they are the most common primary intracranial tumor. Ginsenoside CK (GS-CK) is converted from the diol ginsenoside. This study aimed to explore the effects of GS-CK on glioma cells SHG-44 and U251MG in order to provide clinical value for the treatment of gliomas. Materials and Methods: Cell proliferation was detected using the CCK-8 and CFU detection experiments. Cell apoptosis was detected by DAPI and acridine orange/ethidium bromide (AO/EB) fluorescence staining. Cell scratch and transwell assay were used to detect the effect of GS-CK on cell migration and invasion ability. Apoptosis-related protein expression was detected in the two cell lines after treatment with GS-CK. Results: Cell proliferation is obviously inhibited, and cell migration and invasion were also significantly inhibited by GS-CK. It also induced cell apoptosis in a time- and dose-dependent manner. GS-CK induced significant changes in mitochondrial apoptosis pathway-related protein expression of cytochrome C, p53, Bax, Bcl-2, Caspase-3/8/9, Cleaved Caspase-3, and MMP-9 in glioma cells. Conclusion: GS-CK can inhibit glioma cells by regulating mitochondria-related apoptosis p53-bax-caspases pathway.