Hymeglusin Induces Apoptosis and G0/G1 Cycle Arrest in LX-2 Cells
CHANG Xueting1,2, WEI Mingyue2, HE Jianlin2, WU Kefeng1, XU Guangxin2, TANG Xixiang1,2*
This study investigated the effects of hymeglusin on the human hepatic stellate cell line LX-2. The CCK-8 assay was used to investigate the impact of different concentrations of hymeglusin on the viability of LX-2 cells, as well as to examine the effects of various death inhibitors and hymeglusin on LX-2 cells viability. Flow cytometry was used to evaluate apoptosis in LX-2 cells treated with different concentrations of hymeglusin, CQ (chloroquine), or hymeglusin plus CQ. RNA-seq analysis identified differentially expressed genes between control and hymeglusin-treated groups, followed by GO enrichment and KEGG pathway analyses. Cell-cycle alterations after hymeglusin treatment were also examined by flow cytometry. The results showed that, compared with the control group, 40 μmol/L hymeglusin markedly reduced LX-2 cells viability. Hymeglusin-induced LX-2 cells death occurred primarily via apoptosis. CQ potentiated hymeglusin-mediated apoptosis, whereas Z-VAD-FMK partially reversed this CQ-enhanced pro-apoptotic effect. KEGG pathway analysis revealed that significantly dif- ferentially expressed genes in the cell cycle pathway showed a downregulation trend. Hymeglusin treatment significantly increased the proportion of LX-2 cells in G0/G1 phase and decreased the proportion in G2/M phase; combined treatment with CQ further induced G2/M arrest. Collectively, hymeglusin induces apoptosis and G0/G1 phase arrest in LX-2 cells, and CQ further enhances this pro-apoptotic effect.
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