ABSTRACT
Objective:To determine the role and molecular mechanism of dexmedetomidine (DEX) in postmenopausal osteoporosis (PMOP) .Methods:Twenty-seven patients with PMOP admitted to Yantai Yantaishan Hospital from Jan. 2020 to Jan. 2021 were selected as PMOP group, and 20 healthy volunteers were selected as Normal group. The differentially expressed miRNAs in PMOP were screened, clinically, the expression of miR-483-3p and catenin beta 1 (CTNNB1) in serum samples of patients with PMOP was detected by qRT-PCR. In vitro experiment, Bone marrow mesenchymal stem cells (BMSCs) were induced into osteoblasts, Dex was used to treat BMSCs and intervene the expression of miR-483-3p, CTNNB1 in BMSCs, the expression level of osteogenesis related indexes (RUNX2、OCN、OPN) was detected. After coculturing Human umbilical vein endothelial cell (HUVECs) with BMSCs, angiogenesis experiment was utilized to detect the angiogenesis ability.Results:Compared with Normal group (1±0.46) (1.03±0.44) , the expression of miR-483-3p (3.23±1.61) was increased in serum of PMOP patients while expression of CTNNB1 (0.50±0.27) was inhibited ( t=5.99, P<0.001) ( t=5.14, P<0.001) . miR-483-3p has a good diagnostic effect on PMOP (AUC=0.86, P<0.001) . After Dex treatment, miR-483-3p level was decreased in BMSCs, CTNNB1 level was increased (all P<0.05) . Dex promoted the expression of RUNX2, OCN, OPN and number of angiogenesis, but this effect was partially reversed by miR-483-3p overexpression (all P<0.05) . CTNNB1 was confirmed as a target gene of miR-483-3p, the inhibition effects of miR-483-3p overexpression on osteogenic differentiation and angiogenesis of BMSCs induced by Dex was partially reversed by CTNNB1 overexpression (all P<0.05) . Conclusion:Dex enhanced CTNNB1 level in PMOP via inhibiting miR-483-3p, subsequently promoted osteogenic differentiation and angiogenesis of BMSCs and inhibited progression of PMOP.
ABSTRACT
Objective:To explore the effects and molecular mechanism of circ_001598 on biological behavior of breast cancer (BC) cells.Methods:Sevoflurane in different concentrations were used to treat BC cells and the cell activity and apoptosis were detected. qRT-PCR was used to determine the relative expression of Circ_001598 and miR-588 in BC tissue and cells. The effects of Sevoflurane on Circ_001598, miR-588 expression was detected. Dual luciferase reporter gene assay was used to detect the relationship between Circ_001598 and miR-588. The expression of Circ_001598, miR-588 in BC cells was intervened, then cell activity and apoptosis level was detected by using MTT and flow cytometry individually.Results:Sevoflurane inhibited cell activity of BC cells, and promoted cell apoptosis. Circ_001598 was increased in BC tissue and cells, but Sevoflurane could down-regulate the expression of Circ_001598 (all P<0.05) . Overexpression of Circ_001589 partially saved the effects of Sevoflurane on cell viability and apoptosis. Circ_001598 negatively regulated miR-588 in BC cells. miR-588 expression was down-regulated in BC tissue and cells, but Sevoflurane up-regulated the expression level of miR-588 in BC cells (all P<0.05) . miR-588 transfection partially offseted the effects of Circ_001598 on Sevoflurane induced BC cells apoptosis. Conclusion:Sevoflurane affects BC cell viability and apoptosis via regulating Circ_001589/miR-588.