Research On The Effect Of Proliferation Inhibition And Autophagy Regulation Of Glioma Cells By Elemene

Objective:To investigate the inhibitory effect of elemicin on the proliferation of glioma cell lines and its effect,to clarify whether elemicin has an autophagy-regulating effect on glioma cell lines and its mechanism,and to provide a theoretical basis for the clinical application and in-depth study of elemicin in glioma patients.Methods:The effects of different concentrations of β-elemene on the proliferation and migration ability of glioma U87 and U251 cell lines were observed by CCK8 cell proliferation-toxicity assay and cell scratching assay;Glioma U87 and U251 cell lines were treated with different concentrations of β-elemene(0,50,100 μmol/L)for 24 h.The effects of β-elemene on the expression levels of microtubule-associated protein 1 light chain 3(LC3)m RNA,autophagy key molecule yeast Atg6 homolog(Beclin1)m RNA were detected by real-time quantitative polymerase chain reaction(Rt-q PCR);U87 and U251 cells were treated with different concentrations of β-elemene(0,50 and 100μmol/L)for 24 h,and the expression of autophagy-related protein LC3 B and Beclin 1 was detected by Western Blot immunoblotting assay.Results:The results of proliferation-toxicity assay and cell scratch assay of CCK8 cells showed that β-elemene inhibited the proliferation and migration of U87 and U251 glioma cells;Real-time fluorescence quantitative PCR results showed that β-elemicene increased the expression levels of LC3 m RNA and Beclin1 m RNA in U87 and U251 glioma cells after treatment with different concentrations of β-elemicene compared with the control group(P < 0.05);Western Blot assay showed that the expression levels of autophagy-related proteins LC3B-II and Beclin 1 were increased in U87 and U251 cells in the β-elemene treated group compared with the control group(P < 0.05).Conclusion:In the present study,we found that β-elemene dose-dependently inhibited the proliferation and migration of U87 and U251 glioma cells.β-elemene may regulate the autophagy of glioma cells by increasing the expression of autophagy-related proteins LC3B-II and Beclin 1 and increasing the expression levels of LC3 m RNA and Beclin 1m RNA.