Objective: To study the potential targets and mechanisms of curcumol against glioma using network pharmacology and in vitro experiments, and to provide theoretical basis for its clinical application and scientific research. Methods: TCMSP database and Swiss database were used to screen the potential targets, geneCards database and OMIM database were used to obtain glioma-related targets. The intersection targets of curcumol-glioma were obtained and the Wayne diagram was drawn. The PPI network was constructed using STRING database and the core targets were screened. Metascape database was used for GO and KEGG enrichment analysis to further explore the pharmacological mechanism of curcumol against glioma. Finally, MTT method was used to detect the proliferation effect of curcumol on glioma U87 cells, and western blot was used to detect the expression levels of PI3K, p-AKT and AKT proteins, to further confirm the results of network pharmacology analysis. Results: A total of 4 821 glioma targets were obtained from 102 potential targets predicted by curcumol. There were 67 intersection targets between curcumol and glioma, and the main core targets were MAPK1, EGFR, MAPK8, MAPK14 and JAK3. GO enrichment analysis showed 1 003 biological processes, including 854 BFs, 72 MFs, and 77 CCs. KEGG analysis showed 136 signaling pathways, among which PI3K / AKT pathway may play a key role in anti-glioma. Molecular docking showed that zedoaryl could spontaneously combine with EGFR, JKA3, MAPK1, MAPK8 and MAPK to form a relatively stable conformation. The results showed that the inhibitory activity of curcumol on the proliferation of glioma U87 cells was significantly enhanced in a time-and concentration-dependent manner with the increase of concentration. WB results showed that curcumol could reduce the expression of p-AKT protein in glioma U87 cells to inhibit the PI3K / AKT pathway (P＜0.01). Conclusion: Curcumol could inhibit malignant glioma with multiple targets and multiple pathways, and its mechanism may be related to the regulation of p-AKT protein expression.
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