The effect of knockdown of FCGBP on apoptosis and expression of inflammatory factors in SH-SY5Y cells induced by Aβ25-35

DONG Shuai; JIN Xiaohua; YANG Lijun; CHEN Li; LI Xianghua

doi:10.3969/j.issn.2096-9058.2025.03.012

Abstract：Objective To investigate the role of FCGBP in Aβ25-35-induced apoptosis and inflammation in SH-SY5Y cells.Methods The GSE3300 data set in GEO database was selected to analyze and screen the differentially expressed molecules in Alzheimer's disease(AD)tissues.SH-SY5Y cells were induced with 0,5,10 and 20 μmol/L amyloid-β pro-tein 25-35(Aβ25-35)for 24 h,and the expression of FCGBP was detected by Western blotting to determine the optimal con-centration of Aβ25-35 for constructing AD cell model in vitro.Subsequently,si-FCGBP and its negative control si-NC were transfected into SH-SY5Y cells,and treated with 20 μmol/L Aβ25-35 for 24 h.The transfection efficiency was evaluated by Western blotting.The cell viability was detected by CCK-8.Annexin V-FITC/PI and Western blotting were used to detect apoptosis and apoptosis-related protein expression.ELISA was used to detect the inflammatory factors in cell supernatant.Results Analysis of GSE3300 data set showed that the expression of FCGBP in AD tissues was significantly higher than that in normal tissues(P<0.05).Treatment of SH-SY5Y cells with 20 μmol/L Aβ25-35 for 24 h was the best condition for AD cell modeling.Knockdown of FCGBP promoted the viability of SH-SY5Y cells induced by Aβ25-35 reduced the apoptosis rate of cells,up-regulated Bcl-2,down-regulated Bax and cleaved Caspase3,and inhibited the expression of inflammatory factors IL-1,IL-6,IL-18 and TNF-α(all P<0.05).Conclusions FCGBP is highly expressed in AD brain tissue.Knockdown of FCGBP promotes the viability of SH-SY5Y cells induced by Aβ25-35,inhibits apoptosis and reduces the re-lease of inflammatory factors.