Ground-level ozone is an irritant and is harmful to human respiratory and nervous systems. Thus, four manganese oxides with different crystals were hydrothermally synthesized to decompose residual ozone (deO₃) in an ozone synergistic–oxidation system. Among them, a cactus-like MnO₂-IV nanosphere exhibited the highest deO₃ activity, with excellent tolerance to water vapor and SO₂/H₂O, which could maintain >88% deO₃ efficiency in the high-humidity and sulfur-containing conditions. It benefits from the unique morphology, high specific surface area, superior redox properties, oxygen chemisorption capabilities, abundant surface-active hydroxyl species, and low valence Mn species. More importantly, the detailed interference mechanism of O₂/O₃/H₂O/SO₂ molecules on MnO₂-IV was revealed utilizing in situ diffused reflectance infrared Fourier transform spectroscopy and X-ray photoelectron spectroscopy. H₂O generally caused recoverable deactivation, but that caused by SO₂ was irreversible. The synergistic effect of SO₂/H₂O promoted the formation of an unstable sulfate species, thereby deepening the deactivation but inhibiting the irreversible poisoning. Finally, nine specific steps to decompose ozone via surface-active hydroxyl/intermediates were established.

NO oxidation was conducted over MnO_x-CeO₂ catalysts, which were synthesized by the co-precipitation method. The calcination temperature and third metal doping were the main considerations. MnCe catalysts calcined at 350 °C and 450 °C attained the highest NO conversion efficiency, compared to 550 °C. XRD results suggested that the higher the calcination temperature, the higher the crystallization degree, which led to a negative effect on catalytic activity. Subsequently, Sn, Fe, Co, Cr, and Cu were separately doped into MnCe composites, but no improvement was observed for these trimetallic catalysts in NO conversion. Nevertheless, MnCeSn, MnCeFe, and MnCeCo still exhibited a desirable NO conversion efficiency, so they were tested under SO₂ addition together with MnCe catalyst. Among them, MnCeFe exhibited the highest NO conversion after whole poisoning testing. XPS results indicated that Fe could protect Mn and Ce metal oxides from being reduced during SO₂ poisoning process. Furthermore, in in-situ DRIFTS measurement, part of nitrate species maintained undestroyed on the MnCeFe catalyst surface after SO₂ poisoning. These characteristics reinforced that Fe dropping would achieve better performance under SO₂ atmosphere.

Aneurysm (AN) embolization is an important treatment for cerebral aneurysms. The endothelialization of the aneurysm neck is crucial for preventing aneurysm recurrence. Sitagliptin is a therapeutic drug for diabetes that has been reported to have cardiovascular-protective effects. This study investigated the effect of sitagliptin on endothelial progenitor cell (EPC) function and endothelialization of aneurysm necks after embolization. The effect of sitagliptin on aneurysm neck endothelialization was examined using a rat aneurysm embolization model. We isolated EPCs and used CCK-8 (Cell Counting Kit-8) and annexin V/PI to analyze the effect of sitagliptin on the proliferation and apoptosis of EPCs. The effects of sitagliptin on the migration and invasion of EPCs were examined using scratch and Transwell assays. The effect of sitagliptin on the angiogenic ability of EPCs was examined using a sprouting assay. Western blot analysis and ELISA were used to analyze the effect of sitagliptin on the expression of proangiogenic factors in EPCs. The in vivo results indicated that sitagliptin promoted endothelialization of the aneurysm neck and increased circulating EPCs and expression levels of SDF-1 and VEGF in peripheral blood. Sitagliptin promoted the proliferation, migration, invasion, and angiogenic abilities of EPCs. Western blot analysis and ELISA showed that sitagliptin promoted the expression of SDF-1 and VEGF in progenitor endothelial cells. Western blot assays showed that sitagliptin activated the expression of NRF2, which is dependent on the function of CXCR4. Furthermore, sitagliptin promoted progenitor endothelial cell migration, invasion and angiogenesis through the SDF-1/CXCR4/NRF2 signaling pathway. Additionally, progenitor endothelial cells expressed SDF-1 and VEGF. The promotion of endothelialization by sitagliptin provides an additional therapeutic option for preventing the recurrence of AN.