Publication | Open Access
<i>Panax notoginseng</i> Saponins Attenuate Oxygen–Glucose Deprivation/Reoxygenation-Induced Injury in Human SH-SY5Y Cells by Regulating the Expression of Inflammatory Factors through miR-155
24
Citations
19
References
2018
Year
ImmunologyCell DeathCell CycleRedox BiologyCellular PhysiologyOxidative StressNeuroinflammationInflammationInflammatory FactorsHuman Sh-sy5y CellsNeurologyPanax Notoginseng SaponinsNeuroimmunologyCell SignalingIschemic SyndromeMolecular SignalingRedox SignalingMolecular PhysiologyMedicineChronic InflammationVascular BiologyImmune FunctionPns-induced DecreasesCerebral Blood FlowGene ExpressionEpigenetic RegulationCell BiologyReperfusion InjuryMicrorna DetectionReactive Oxygen SpecieIschemic StrokeStrokePanax Notoginseng
Panax notoginseng saponins (PNS) have been widely used in China to treat stroke. Accumulating evidence has found that microRNA (miR)-155 plays critical roles in the pathology of ischemic stroke. Here we investigated whether PNS plays a protective effect against oxygen-glucose deprivation/reoxygenation (OGD/R)-induced focal inflammation and injury in SH-SY5Y cells by regulating miR-155 expression. Treatment with PNS at a concentration less than 160 µg/mL had no effect on the proliferation of SH-SY5Y cell. In OGD/R-induced SH-SY5Y cells, 160 µg/mL PNS treatment promoted cell proliferation and cell cycle progression, as well as decreased inhibited apoptosis and miR-155 expression. However, overexpression of miR-155 attenuated the promotion effects of PNS on cell proliferation and cell cycle, apoptosis inhibition in OGD/R-induced SH-SY5Y cells. Moreover, 160 µg/mL PNS treatment decreased the levels of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) in OGD/R-induced SH-SY5Y cells, whereas overexpression of miR-155 reversed PNS-induced decreases in the levels of IL-1β, IL-6, and TNF-α in OGD/R-treated SH-SY5Y cells. In conclusion, PNS attenuated OGD/R-induced injury in human undifferentiated SH-SY5Y cells by regulating the expression of inflammatory factors through miR-155.
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