Abstract: Objective To investigate the effect of liensinine (LI) on apoptosis of U251 gliomacells and its mechanisms. Methods U251 and HEB cells were treated with different concentrationsof LI for 24 / 48 h, CCK8 assay and colony formation assay were performed to detect cell viability, flow cytometer was performed to detect apoptosis, and the expression levels of apoptotic proteins (Bax / Bcl-2, cleaved PARP) were detected by Western blotting. Cells were divided into 6 groups: control, LI, NAC, LI + NAC, SP600125, LI + SP600125. ROS was detected by DCFH-DA and p-JNK / cleaved PARP by Western blotting. U251 xenograft model was established to evaluate theeffect of LI on tumor volume / weight and tumor cell apoptosis. Results LI significantly inhibited theproliferation of U251 cells, decreased the colony formation of U251 cells, and promoted apoptosis. LI (80 μmol / L) induced ROS production and JNK phosphorylation, which were reversed byNAC and SP600125. In vivo experiments showed that LI inhibited tumor growth, reduced Ki67 positive cells, and promoted apoptosis. Conclusion LI selectively inhibits U251 via ROS / JNK-mediated apoptosis, demonstrating therapeutic potential for glioma.

Key words: glioma, liensinine, apoptosis, autophagy, LC3B