Objective:To explore the regulatory mechanism of OIP5-AS1 in chronic periodontitis(CP).Methods:Human perio-dontal ligament stem cells(PDLSC)were treated with LPS to establish an in vitro model of CP.Real-time quantitative polymerase chain reaction(qRT-PCR)was performed to detect the expression of OIP5-AS1,miR-143-3p and fibroblast growth factor 1(FGF1)mRNA in periodontal ligament tissues and PDLSCs of CP patients and healthy volunteers.3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide(MTT)method was performed to detect cell viability.Enzyme-linked immunosorbent assay(ELISA)was performed to measure the levels of inflammatory cytokines interleukin-1 β(IL-1 β),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α).Western blot was performed to detect Bax,Bcl-2 and FGF1 protein levels.A dual-luciferase reporter assay was performed to validate the targeting relationship between miR-143-3p and OIP5-AS1/FGF1.Results:The expression of OIP5-AS1 and FGF1 were decreased,and the expression of miR-143-3p was increased in CP patients and LPS-treated PDLSCs(P＜0.05).In LPS-treated PDLSCs,OIP5-AS1 overexpression promoted cell viability and inhibited inflammation and apoptosis(P＜0.05).In addition,OIP5-AS1 targeted miR-143-3p and negatively regulated miR-143-3p expression(P＜0.05).In LPS-treated PDLSCs,up-regulation of miR-143-3p attenuated the inhibitory effect of OIP5-AS1 overexpression on LPS-induced PDLSC dam-age(P＜0.05).miR-143-3p targeted FGF1 and negatively regulated FGF1 expression(P＜0.05).FGF1 overexpression attenuated the effect of co-overexpression of miR-143-3p and IP5-AS1 on LPS-induced damage(P＜0.05).Conclusion:OIP5-AS1 may at-tenuate LPS-induced PDLSC inflammatory response and apoptosis and enhance cell viability by regulating the miR-143-3p/FGF1 axis,which may provide a new target for CP therapy.

Objective:To explore the regulatory mechanism of OIP5-AS1 in chronic periodontitis(CP).Methods:Human perio-dontal ligament stem cells(PDLSC)were treated with LPS to establish an in vitro model of CP.Real-time quantitative polymerase chain reaction(qRT-PCR)was performed to detect the expression of OIP5-AS1,miR-143-3p and fibroblast growth factor 1(FGF1)mRNA in periodontal ligament tissues and PDLSCs of CP patients and healthy volunteers.3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide(MTT)method was performed to detect cell viability.Enzyme-linked immunosorbent assay(ELISA)was performed to measure the levels of inflammatory cytokines interleukin-1 β(IL-1 β),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α).Western blot was performed to detect Bax,Bcl-2 and FGF1 protein levels.A dual-luciferase reporter assay was performed to validate the targeting relationship between miR-143-3p and OIP5-AS1/FGF1.Results:The expression of OIP5-AS1 and FGF1 were decreased,and the expression of miR-143-3p was increased in CP patients and LPS-treated PDLSCs(P＜0.05).In LPS-treated PDLSCs,OIP5-AS1 overexpression promoted cell viability and inhibited inflammation and apoptosis(P＜0.05).In addition,OIP5-AS1 targeted miR-143-3p and negatively regulated miR-143-3p expression(P＜0.05).In LPS-treated PDLSCs,up-regulation of miR-143-3p attenuated the inhibitory effect of OIP5-AS1 overexpression on LPS-induced PDLSC dam-age(P＜0.05).miR-143-3p targeted FGF1 and negatively regulated FGF1 expression(P＜0.05).FGF1 overexpression attenuated the effect of co-overexpression of miR-143-3p and IP5-AS1 on LPS-induced damage(P＜0.05).Conclusion:OIP5-AS1 may at-tenuate LPS-induced PDLSC inflammatory response and apoptosis and enhance cell viability by regulating the miR-143-3p/FGF1 axis,which may provide a new target for CP therapy.