Combined Scutellarin and CHNO Imperils the Survival of Glioma: Partly Associated With the Repression of PSEN1/PI3K-AKT Signaling Axis.

Glioma, the most common intracranial tumor, harbors great harm. Since the treatment for it has reached the bottleneck stage, the development of new drugs becomes a trend. Therefore, we focus on the effect of scutellarin (SCU) and its combination with CHNO (abbreviated as ) on glioma and its possible mechanism in this study. Firstly, SCU and CHNO both suppressed the proliferation of U251 and LN229 cells in a dose-dependent manner, and CHNO augmented the inhibition effect of SCU on U251 and LN229 cells . Moreover, there was an interactive effect between them. Secondly, SCU and CHNO decreased U251 cells in G2 phase and LN229 cells in G2 and S phases but increased U251 cells in S phase, respectively. Meanwhile, the combination could further reduce U251 cells in G2 phase and LN229 cells in G2 and S phases. Thirdly, SCU and CHNO both induced the apoptosis of U251 and LN229. The combination further increased the apoptosis rate of both cells compared with the two drugs alone. Furthermore, SCU and CHNO both inhibited the lateral and vertical migration of both cells, which was further repressed by the combination. More importantly, the effect of SCU and the combination was better than positive control-temozolomide, and the toxicity was low. Additionally, SCU and CHNO could suppress the growth of glioma , and the effect of the combination was better. Finally, SCU and the combination upregulated the presenilin 1 (PSEN1) level but inactivated the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT) signaling and . Accordingly, we concluded that scutellarin and its combination with CHNO suppressed the proliferation/growth and migration and induced the apoptosis of glioma, in which the mechanism might be associated with the repression of PSEN1/PI3K-AKT signaling axis.