Acteoside Presents Protective Effects on Cerebral Ischemia/reperfusion Injury Through Targeting CCL2, CXCL10, and ICAM1.

The objective of this study is to investigate the roles of acteoside (ACT) in cells with oxygen-glucose deprivation and reoxygenation (OGD/R)-induced injury and the underlying mechanisms. The differentially expressed genes (DEGs) in rats with middle cerebral artery occlusion were identified using GSE61616 data set. Kyoto Encyclopedia of Genes and Genomes pathway enrichment with the DEGs and the prediction of ACT's targets were conducted using The Comparative Toxicogenomics Database. The OGD/R model was established with bEnd.3 cells. Following that, bEnd.3 cells were treated by distinct concentrations of ACT and IL-10. The proliferation and apoptosis of cells were analyzed by cell counting kit-8 and flow cytometry assays, respectively. Western blot was used to check involved proteins. Herein, we identified CCL2, CXCL10, and ICAM1 as the targets of ACT, which were upregulated in tissues of MACO rats and cells with OGD/R-induced injury. ACT promoted the proliferation but reduce the apoptosis of cells with OGD/R-induced injury. Moreover, these effects of ACT were enhanced by IL-10. After being treated with ACT, IL-10, or ACT together with IL-10, the levels of CCL2, CXCL10, and ICAM1 were all decreased, whereas p-Stat3 was raised in cells with OGD/R-induced injury, while Stat3 expression presented no significant difference among groups. ACT protected cells against OGD/R-induced injury through regulating the IL-10/Stat3 signaling, indicating that ACT might be an effective therapy drug to lower cerebral ischemia/reperfusion injury.