RESUMEN
The Fenton reaction, induced by the H2O2 formed during the oxygen reduction reaction (ORR) process leads to significant dissolution of Fe, resulting in unsatisfactory stability of the iron-nitrogen-doped carbon catalysts (Fe-NC). In this study, a strategy is proposed to improve the ORR catalytic activity while eliminating the effect of H2O2 by introducing CeO2 nanoparticles. Transmission electron microscopy and subsequent characterizations reveal that CeO2 nanoparticles are uniformly distributed on the carbon substrate, with atomically dispersed Fe single-atom catalysts (SACs) adjacent to them. CeO2@Fe-NC achieves a half-wave potential of 0.89 V and a limiting current density of 6.2 mA cm-2, which significantly outperforms Fe-NC and commercial Pt/C. CeO2@Fe-NC also shows a half-wave potential loss of only 1% after 10 000 CV cycles, which is better than that of Fe-NC (7%). Further, H2O2 elimination experiments show that the introduction of CeO2 significantly accelerate the decomposition of H2O2. In situ Raman spectroscopy results suggest that CeO2@Fe-NC significantly facilitates the formation of ORR intermediates compared with Fe-NC. The Zn-air batteries utilizing CeO2@Fe-NC cathodes exhibit satisfactory peak power density and open-circuit voltage. Furthermore, theoretical calculations show that the introduction of CeO2 enhances the ORR activity of Fe-NC SAC. This study provides insights for optimizing SAC-based electrocatalysts with high activity and stability.
RESUMEN
BACKGROUND: Disc degeneration is correlated with mechanical load. Osteogenic protein-1 (OP-1) is potential to regenerate degenerative disc. OBJECTIVE: To investigate whether OP-1 can protect against high magitude compression-induced nucleus pulposus (NP) cell apoptosis and NP matrix catabolism, and its potential mechanism. METHODS: Porcine discs were cultured in a bioreactor and compressed at a relatively high-magnitude mechanical compression (1.3 MPa at a frequency of 1.0 Hz for 2 hours once per day) for 7 days. OP-1 was added along with the culture medium to investigate the protective effects of OP-1. NP cell apoptosis and matrix biosynthesis were evaluated. Additionally, activity of the p38 MAPK pathway is also analyzed. RESULTS: Compared with the control group, high magnitude compression significantly promoted NP cell apoptosis and decreased NP matrix biosynthesis, reflected by the increase in the number of TUNEL-positive cells and caspase-3 activity, the up-regulated expression of Bax and caspase-3 mRNA and down-regulated expression of Bcl-2 mRNA, and the decreased alcian blue staining intensity and expression of matrix proteins (aggrecan and collagen II). However, OP-1 addition partly attenuated the effects of high magnitude compression on NP cell apoptosis and NP matrix biosynthesis. Further analysis showed that inhibition of the p38 MAPK pathway partly participated in this process. CONCLUSION: OP-1 can attenuate high magnitude compression-induced NP cell apoptosis and promoted NP matrix biosynthesis, and inhibition of the p38 MAPK pathway may participate in this regulatory process. This study provides that OP-1 may be efficacy in retarding mechanical overloading-exacerbated disc degeneration.
