Sevoflurane downregulates insulin-like growth factor-1 to inhibit cell proliferation, invasion and trigger apoptosis in glioma through the PI3K/AKT signaling pathway.

Abstract

Sevoflurane is a new type of inhalation anesthetic used widely in the clinic. It has the characteristics of rapid induction, rapid recovery, and less irritative to the airway. Studies have shown that sevoflurane can affect the invasion and migration of a variety of malignant tumors. However, its effects on human glioma cells and related mechanisms are not clear. Cultured U251 and U87 cells were pretreated with sevoflurane. The effect of sevoflurane on proliferation was evaluated by MTT, and cell migration assay, cell apoptosis, and invasion ability were evaluated by wound-healing assay, cell apoptosis, and Transwell assays. Insulin-like growth factor-1 (IGF-1) and PI3K/AKT signaling pathway gene expression in sevoflurane-treated cell lines was measured by western blotting analysis, respectively. 5% sevoflurane significantly inhibited proliferation ability in both U251 and U87 cells. Sevoflurane inhibited glioma cells invasion and migration, and promoted apoptosis. Sevoflurane inhibited IGF-1 and promoted the expression of apoptosis-related proteins in glioma cells. In addition, sevoflurane inhibited the PI3K/AKT signaling pathway in glioma cells. This study clarifies that sevoflurane inhibits proliferation, invasion, and migration, and promotes apoptosis in glioma cells. These effects are regulated by IGF-1, an upstream gene of the PI3K/AKT signaling pathway. These findings may be significant for the selection of anesthetic agents in glioma surgery to improve the prognosis of patients.