Inhibition of LPS-induced Macrophage Injury by Acacetin via Regulating NF-κB Signaling Pathway
Objective:To explore the anti-inflammatory mechanisms of acacetin in lipopolysaccharide(LPS)-induced mouse bone marrow-derived macrophages(BMDMs).Methods:The effect of various concentrations of acacetin(5,10,20,and 40 μmol/L)on the proliferation of BMDMs was tested using the CCK-8 method,so as to select the optimal dosage.BMDMs were isolated and cul-tured,and LPS(50 ng/mL)was used to pretreat BMDMs for 0,10,30,and 60 minutes.Then,BMDMs were added with acacetin(10 µmol/L)and cultured for 0.5 h.Western blotting was used to analyze the expression of phosphorylated p65(p-p65),p65,nuclear factor(NF)κB suppressor protein α(IκBα),and phosphorylated IκBα(p-IκBα).The nuclear translocation of NF κB was detected by laser scanning confocal microscope(LSCM).Results:CCK-8 results showed that acacetin concentrations ranging from 5 to 40 µmol/L had no significant effect on the proliferation of BMDMs.Based on previous studies of the team,10 µmol/L of acacetin was chosen for subsequent experiments.Compared with the blank control group,LPS stimulation significantly increased the expression levels of p-p65 and p-IκBα.Treatment with acacetin significantly reduced the expression levels of p-NF-κB p65 and p-Iκ Bα.More-over,acacetin inhibited the LPS-induced nuclear translocation of NF-κB p65.Conclusion:The anti-inflammatory effects of acacetin were related to the inhibition of the NF-κB signaling pathway,suggesting acacetin may be a potential anti-inflammatory drug.
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