ADSCs regulate neuronal survival and inflammatory response through PI3K/Akt and NF-κB pathways
Objective This study aimed to investigate the neuroprotective effects and mechanisms of adipose-derived mesenchymal stem cells(ADSCs)on neurons in vitro.Methods Primary ADSCs were cultured and identified,and a glutamate-induced HT22 neuronal cell injury model was established.Cell immunofluorescence was used to detect changes in the number and length of branches in the injured HT22 model.Co-cultures of ADSCs and HT22 were established to examine the regulatory effects of ADSCs on HT22 cell apoptosis.ELISA was employed to study the impact of ADSCs on inflammatory factors(TNF-α,IL-1 β,IL-6,IL-10)in injured HT22 cells.Western blot analysis was performed to investigate changes in PI3K/Akt and NF-κB phosphorylation,exploring the mechanisms of ADSCs action on injured HT22.Results Cell immunofluorescence confirmed that enzymatic culture of ADSCs expressed high levels of CD44.Compared to the control group,cytotoxicity assays indicated a gradual decrease in HT22 cell survival with increasing glutamate concentration,reaching 20mM as the half-maximal inhibitory concentration.At this concentration,HT22 branch number and length significantly decreased.ADSCs effectively reduced glutamate-induced HT22 cell apoptosis and decreased cleaved caspase3 expression compared to the Glu group.ELISA results showed that ADSCs significantly decreased the expression of pro-inflammatory factors in injured HT22 cells while increasing the level of the anti-inflammatory factor IL-10.ADSCs regulated neuronal survival and inflammatory responses through promoting PI3K/Akt phosphorylation and inhibiting NF-K B phosphorylation.Conclusion ADSCs demonstrate significant neuroprotective effects,promoting the survival and functional recovery of damaged neurons by modulating key signaling pathways.This discovery provides new research directions and hope for the treatment of spinal cord injuries(SCI).
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