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Acteoside Presents Protective Effects on Cerebral Ischemia/reperfusion Injury Through Targeting CCL2, CXCL10, and
Weijiang Wu1, Gang Wu2, Deyan Cao3
1Department of Neurosurgery, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu Province, PR China.
Abstract:
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.
Insights
Acteoside (ACT) protects cells from oxygen-glucose deprivation and reoxygenation (OGD/R) injury by reducing apoptosis and enhancing proliferation. ACT regulates the IL-10/Stat3 pathway, suggesting its potential as a therapeutic for cerebral ischemia/reperfusion injury.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Cerebral ischemia/reperfusion injury is a significant cause of neurological damage.
- Oxygen-glucose deprivation and reoxygenation (OGD/R) models are used to study cellular injury mechanisms.
- Identifying novel therapeutic targets for OGD/R-induced injury is crucial.
Purpose of the Study:
- To investigate the protective effects of acteoside (ACT) on cells experiencing OGD/R-induced injury.
- To elucidate the underlying molecular mechanisms of ACT's action, focusing on the IL-10/Stat3 signaling pathway.
Main Methods:
- Differential gene expression analysis (GSE61616) and pathway enrichment (Kyoto Encyclopedia of Genes and Genomes) were used to identify targets.
- An in vitro OGD/R model using bEnd.3 cells was established.
- Cell proliferation, apoptosis, and protein expression (Western blot) were assessed after ACT and IL-10 treatment.
Main Results:
- Acteoside (ACT) was identified as a potential therapeutic agent targeting CCL2, CXCL10, and ICAM1, which are upregulated in OGD/R injury.
- ACT promoted cell proliferation and reduced apoptosis in OGD/R-injured cells, with enhanced effects when combined with IL-10.
- ACT treatment decreased CCL2, CXCL10, and ICAM1 levels while increasing p-Stat3, indicating regulation of the IL-10/Stat3 pathway.
Conclusions:
- Acteoside (ACT) demonstrates significant protective effects against OGD/R-induced cellular injury.
- The mechanism involves the regulation of the IL-10/Stat3 signaling pathway.
- ACT holds promise as a potential therapeutic drug for mitigating cerebral ischemia/reperfusion injury.
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