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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. [ABSTRACT FROM AUTHOR]

Background: Non-small cell lung cancer (NSCLC) is often harmful to human health. It is common in people who smoke or smoke passively, and the affected people are older and find it difficult to recover. The main treatment methods are surgery, radiotherapy and chemotherapy. This paper aims to study the effects of different configurations of ginsenoside Rh2 on NSCLC 95D and NCI-H460 cells. To provide clinical value for the treatment of NSCLC. Materials and Methods: CCK-8 was used to determine the proliferation of 95D and NCI-H460 cells with different concentrations of ginsenoside Rh2 (0, 0.05, 0.1 and 0.2 mg/mL), and IC50 was calculated. Cell cycle and apoptosis were detected by immunofluorescence staining and flow cytometry. Results: 20(R)-ginsenoside-Rh2 and 20(S)-ginsenoside-Rh2 inhibited the proliferation and colony formation of NSCLC 95D and NCI-H460 cells induced cell cycle arrest in a time and dose-dependent manner in G1/S and promote apoptosis. Conclusion: Ginsenoside Rh2 induces antitumour activity by inhibiting proliferation and colony formation of 95D and NCI-H460 cells and inducing cell cycle arrest and apoptosis. Comparing the two configurations of ginsenoside Rh2, the effect of 20(R)-ginsenoside-Rh2 is stronger. [ABSTRACT FROM AUTHOR]