ABSTRACT
The cathodic product Li2CO3, due to its high decomposition potential, has hindered the practical application of rechargeable Li-CO2/O2 batteries. To overcome this bottleneck, a Pt/FeNC cathodic catalyst is fabricated by dispersing Pt nanoparticles (NPs) with a uniform size of 2.4 nm and 8.3 wt % loading amount into a porous microcube FeNC support for high-performance rechargeable Li-CO2/O2 batteries. The FeNC matrix is composed of numerous two-dimensional (2D) carbon nanosheets, which is derived from an Fe-doping zinc metal-organic framework (Zn-MOF). Importantly, using Pt/FeNC as the cathodic catalyst, the Li-CO2/O2 (VCO2/VO2 = 4:1) battery displays the lowest overpotential of 0.54 V and a long-term stability of 142 cycles, which is superior to batteries with FeNC (1.67 V, 47 cycles) and NC (1.87 V, 23 cycles) catalysts. The FeNC matrix and Pt NPs can exert a synergetic effect to decrease the decomposition potential of Li2CO3 and thus enhance the battery performance. In situ Fourier transform infrared (FTIR) spectroscopy further confirms that Li2CO3 can be completely decomposed under a low potential of 3.3 V using the Pt/FeNC catalyst. Impressively, Li2CO3 exhibits a film structure on the surface of the Pt/FeNC catalysts by scanning electron microscopy (SEM), and its size can be limited by the confined space between the carbon sheets in Pt/FeNC, which enlarges the better contacting interface. In addition, density functional theory (DFT) calculations reveal that the Pt and FeNC catalysts show a higher adsorption energy for Li2CO3 and Li2CO4 intermediates compared to the NC catalyst, and the possible discharge pathways are deeply investigated. The synergetic effect between the FeNC support and Pt active sites makes the Li-CO2/O2 battery achieve optimal performance.
ABSTRACT
OBJECTIVE: Toll-like receptors (TLRs) pathway has been demonstrated to play an important role in periodontitis. However, the regulatory mechanism of microRNAs (miRNAs) on TLRs pathway is still unclear. Hence, this study is to explore the function of miRNA-146a in inflammatory reaction induced by Porphyromonas gingivalis lipopolysaccharide (LPS) in human periodontal ligament cells (hPDLCs). METHODS: Cells were treated with 1 or 10 µg/ml P. gingivalis LPS. The expression of TLR2, TLR4 and miRNA-146a were measured by real-time polymerase chain reaction (PCR). Enzyme-linked immunosorbent assay (ELISA) was applied to detect nuclear factor (NF)-κ B p65 nuclear activity, interleukin-1ß (IL-1ß), IL-6, IL-8 and tumor necrosis factor-α (TNF-α). To examine the underlying mechanisms, cells were exposed to anti-TLR2/4 mAb or miRNA-146a inhibitor/mimic and evaluated by real-time PCR and ELISA. RESULTS: 10 µg/ml P. gingivalis LPS increased the expressions of TLR2 (3.79 ± 0.31), TLR4 (2.21 ± 0.31), and miRNA-146a (4.91 ± 0.87), NF-κ B p65 nuclear activity (6.51 ± 0.77 fold) (p < 0.05). 1 µg/ml P. gingivalis LPS induced TLR2 (3.05 ± 0.23), miRNA-146a (3.66 ± 0.83) and NF-κ B p65 nuclear activity (4.06 ± 0.78 fold) (p < 0.05), except TLR4 (1.11 ± 0.30, p > 0.05). Also, cytokines production increased (p < 0.05). The up-regulation of miRNA-146a could be blocked by anti-TLR2/4 mAb (p < 0.05). After the blockage of miRNA-146a, TLR2, TLR4, NF-κ B p65 nuclear activity and proinflammatory cytokines increased. However, after application of miRNA-146a mimic, the levels of these indexes decreased obviously (p < 0.05). CONCLUSION: MiRNA-146a functions as a negative feedback regulator via down-regulating proinflammatory cytokine secretion and blocking TLRs signaling pathway in hPDLCs after P. gingivalis LPS stimulation.