BACKGROUND: Ions doping is an important method for the modification of bioceramic.OBJECTIVE: To evaluate a novel co-substituted bioceramic scaffolds as bone repair material.METHODS: The microstructure and crystallization of the scaffolds were detected by scanning electron microscope and X-ray diffraction. Compression strength test,degradation test and cell culture experiment were assumed to evaluate the properties of KSCPP in vitro. After a short period of muscle pouches implantation,the performance of KSCPP in vivo was evaluated.RESULTS AND CONCLUSION: The results show that KSCPP scaffold has a higher compressive strength and degradation rate. Moreover,the MTT assay and implantation test reveal that the KSCPP scaffold exhibits lower cytotoxicity and better tissue biocompatibility than CPP and HA. The study proved the great potential of KSCPP in bone repair applications.

Objective: To explore the molecular mechanism of docosahexaenoic acid (DHA) on regulating the phenotype switching of hypoxia-induced pulmonary arterial smooth muscle cells (PASMCs). Methods: The PASMCs were isolated from Sprague Dawley rats. PASMCs were divided into five groups: normal control group, hypoxia group (1%O₂, 94%N₂, 5% CO₂ stimulation for 12 hours), hypoxia+ DHA group (10 μmol/L DHA pretreatment followed by 12 hours hypoxia), hypoxia+ DHA+ NFATc1 overexpression group (transfection of the NFATc1 lentivirus for 24 hours, followed by hypoxia stimulation for 12 hours after 10 μmol/L DHA treatment), and hypoxia+ DHA+ siNFATc1 group (transfection the siNFATc1 for 24 hours, followed by hypoxia stimulation for 12 hours after 10 μmol/L DHA treatment). The hypoxia stimulation was achieved by use of a special hypoxia incubator (1%O₂, 94%N₂, 5%CO₂). The expressions of NFATc1 of various groups were determined by qRT-PCR and Western blot. The expression of α-SMA was determined by immunofluorescence staining, qRT-PCR and Western blot. The expression of SM22 was determined by qRT-PCR. The proliferation of PASMC was determined by EDU staining. Results: The mRNA and protein expression levels of NFATc1 were significantly upregulated in hypoxia group compared with the normal control group (P<0.05), while hypoxia-induced upregulation of NFTAc1 could be significantly downregulated by DHA treatment (P<0.05). The α-SMA positive cell number, protein and mRNA levels of α-SMA and the mRNA level of SM22 were significantly lower in the hypoxia group than in normal control group, which could be significantly reversed by DHA, the protective effects could then be abolished by NFATc1 overexpression. Above indices were significantly lower in the hypoxia+ DHA+ siNFATc1 group than in hypoxia+ DHA+ NFATc1 overexpression group (P<0.05). The proliferation of PASMCs was significantly higher in the hypoxia group than in the control group (P<0.05), and which could be significantly reduced by DHA (P<0.05), and the protective effect of DHA could be significantly abolished by overexpression of NFATc1 (P<0.05). The proliferation of PASMCs was significantly lower in the hypoxia+ DHA+ siNFATc1 group than in the hypoxia+ DHA+ overexpression NFATc1 group (P<0.05). Conclusion DHA could prevent hypoxia-induced PASMCs phenotype switching and proliferation by inhibiting NFATc1 signaling.