Objective:To investigate whether the inhibitory effect of berberine (BBR) on inflammation and apoptosis of human dental pulp stem cells (hDPSCs) induced by lipopolysaccharide (LPS) is related to its upregulation of microRNA (miR)-23a.Methods:The 3rd to 4th generation hDPSCs with good growth were taken and randomly divided into the blank control group, LPS group, LPS+ BBR group, LPS+ miR-NC mimics group, LPS+ miR-23a mimics group, and LPS+ BBR+ miR-23a inhibitors group according to the experimental requirements. The expression levels of miR-23a mRNA in each group were detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), and the expression levels of interleukin-1 β(IL-1β), interleukin-6 (IL-6), and tumor necrosis factor -α (TNF-α) in the cell supernatants of each group were detected by enzyme-linked immunosorbent assay (ELISA). The apoptosis rate of cells in each group was detected by flow cytometry, and the expression level of Cleaved caspase-3 of apoptosis-related proteins in each group was detected by Western blot.Results:Compared with the LPS group, different concentrations of LPS+ BBR groups could significantly reduce the expression levels of cellular inflammatory factors IL-1β, IL-6, TNF-α, apoptosis rate, and apoptotic protein Cleaved caspase 3 in a dose-dependent manner (all P<0.05). Compared with the LPS group, the expressions of the cellular inflammatory factors IL-1β, IL-6, TNF-α, apoptosis rate and apoptotic protein Cleaved caspase in the LPS+ miR-23a mimics group, the LPS+ BBR group and the LPS+ BBR+ miR-23a inhibitors group were lower (all P<0.05). Compared with the LPS+ miR-NC mimics group, the cellular inflammatory factors IL-1β, IL-6, TNF-α, apoptosis rate and the expression of apoptotic protein Cleaved caspase 3 in the LPS+ miR-23a mimics group and the LPS+ BBR group were all lower (all P<0.05). Compared with the LPS+ BBR group, the inflammatory factors IL-1β, IL-6, TNF-α, apoptosis rate and the expression of apoptotic protein Cleaved caspase 3 in the LPS+ BBR+ miR-23a inhibitors group were all higher (all P<0.05). Conclusions:BBR can inhibit the inflammatory and apoptotic responses of LPS-induced hDPSCs, which is related to its upregulation of miR-23a expression.

Objective:To investigate whether the inhibitory effect of berberine (BBR) on inflammation and apoptosis of human dental pulp stem cells (hDPSCs) induced by lipopolysaccharide (LPS) is related to its upregulation of microRNA (miR)-23a.Methods:The 3rd to 4th generation hDPSCs with good growth were taken and randomly divided into the blank control group, LPS group, LPS+ BBR group, LPS+ miR-NC mimics group, LPS+ miR-23a mimics group, and LPS+ BBR+ miR-23a inhibitors group according to the experimental requirements. The expression levels of miR-23a mRNA in each group were detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), and the expression levels of interleukin-1 β(IL-1β), interleukin-6 (IL-6), and tumor necrosis factor -α (TNF-α) in the cell supernatants of each group were detected by enzyme-linked immunosorbent assay (ELISA). The apoptosis rate of cells in each group was detected by flow cytometry, and the expression level of Cleaved caspase-3 of apoptosis-related proteins in each group was detected by Western blot.Results:Compared with the LPS group, different concentrations of LPS+ BBR groups could significantly reduce the expression levels of cellular inflammatory factors IL-1β, IL-6, TNF-α, apoptosis rate, and apoptotic protein Cleaved caspase 3 in a dose-dependent manner (all P<0.05). Compared with the LPS group, the expressions of the cellular inflammatory factors IL-1β, IL-6, TNF-α, apoptosis rate and apoptotic protein Cleaved caspase in the LPS+ miR-23a mimics group, the LPS+ BBR group and the LPS+ BBR+ miR-23a inhibitors group were lower (all P<0.05). Compared with the LPS+ miR-NC mimics group, the cellular inflammatory factors IL-1β, IL-6, TNF-α, apoptosis rate and the expression of apoptotic protein Cleaved caspase 3 in the LPS+ miR-23a mimics group and the LPS+ BBR group were all lower (all P<0.05). Compared with the LPS+ BBR group, the inflammatory factors IL-1β, IL-6, TNF-α, apoptosis rate and the expression of apoptotic protein Cleaved caspase 3 in the LPS+ BBR+ miR-23a inhibitors group were all higher (all P<0.05). Conclusions:BBR can inhibit the inflammatory and apoptotic responses of LPS-induced hDPSCs, which is related to its upregulation of miR-23a expression.

Objective:To evaluate the efficacy of cerebral-placental-uterine ratio(CPUR)in predicting late-on-set fetal growth restriction(FGR).Methods:From May 2020 to May 2021,1255 women with singleton pregnancy who underwent prenatal examinations at the University of Hong Kong Shenzhen Hospital were selected for fetal growth and Doppler measurements at 35-37 +6 weeks of gestation.Pregnant women with birth weight of newbo-rns＜the 10th percentile were the FGR group.The pulsatility index(PI)of uterine artery(UtA),umbilical artery(UA)and fetal middle cerebral artery(MCA)were analyzed separately and in combination.ROC curve was used to analyze the cerebral-placental-uterine ratio(CPUR),cerebral-placental ratio(CPR),cerebral-uterine ratio(C-UtA)for predicting late-onset FGR;and to evaluate the sensitivity,positive and negative predictive value and of CPUR in the prediction of late-onset FGR.Results:The area under the curve(AUC)of CPUR,CPR,C-UtA and mean UtA-PI for FGR grope were 0.88,0.86,0.84 and 0.72.Under certain cut-off values and 87% specificity,the specificity of CPUR,CPR,C-UtA and mean UtA-Pifor predicting FGR group was 43.2%,46.6%,39.8% and 23.9%,respectively.The positive predictive values of CPUR,CPR,C-UtA and mean UtA-PI,UA-PI for predicting FGR group were 90.5%,71.9%,83.3%,63.6%and 5.2%,respectively.Conclusions:CPUR is more effective in predicting late onset FGR than CPR,C-UtA and mean UtA-PI.It can effectively increase the detection rate of fetal growth restrictionand reduce the FGR risk.

Objective:To investigate the effects of bromodomain and extraterminal domain (BET) inhibitor JQ1 combined with siPD-L1 on the proliferation and apoptosis of oral squamous cell carcinoma (OSCC) Scc-25 cells and its mechanism.Methods:Scc-25 cells were cultured in vitro and treated with different concentrations of JQ1 (0, 0.2, 1, 5 μmol/L). Cell proliferation was detected by cell count kit-8 (CCK-8) assay; the expression levels of programmed cell death ligand 1(PD-L1) and forkhead box M1(FoxM1) protein were detected by Western blot. Appropriate concentration of JQ1 was selected for subsequent experiments. Scc-25 cells were divided into four groups: control group (without any treatment), siPD-L1 group (transfected with siPD-L1), JQ1 group (added JQ1 after transfected with non-specific siRNA), and combined treatment group (added JQ1 after transfected with siPD-L1). CCK-8 assay was used to detect the proliferation ability of Scc-25 cells in each group. Western blot was used to detect the expression levels of cleaved caspase-3, PD-L1 and FoxM1, and flow cytometry was used to detect the apoptosis rate of cells in each group. Results:With the increase of JQ1 concentration, the proliferation ability of SCC-25 cells and the expression levels of PD-L1 and FoxM1 decreased gradually (all P<0.01). JQ1 concentration of 1 μmol/L had obvious inhibitory effect on cell proliferation and the expression levels of PD-L1 and FoxM1, so JQ1 concentration of 1 μmol/L was selected for subsequent experiments. The proliferation ability of Scc-25 cells, the expression of PD-L1 and FoxM1 proteins in JQ1 group, siPD-L1 group and combination treatment group were significantly lower than those in the control group (all P<0.01), and the expression of cleaved caspase-3 protein and the rate of apoptosis were significantly higher than those in the control group (all P<0.01); Moreover, the effect of the combination treatment group was more significant than that of siPD-L1 group, JQ1 group (all P<0.01). Conclusions:The combination of JQ1 and siPD-L1 could effectively inhibit the proliferation and promotes the apoptosis of OSCC Scc-25 cells, and its mechanism may be related to the suppression of PD-L1 and FoxM1 signaling pathways.