RESUMO
The catalytic oxidation of carbon monoxide (CO) under ambient conditions plays a crucial role in the abatement of indoor CO, which poses risks to human health. Despite the notable activity exhibited by Pt-based catalysts in CO oxidation, their efficacy is usually diminished by the CO self-poisoning issue. In this work, three different Pt/CeO2-based catalysts, which have distinct coordinative environments of Pt but an identical Pt/CeO2 substrate structure, were synthesized by activating the catalyst with CO using different temperatures and durations. Compared with clean and graphite-covered Pt on CeO2, the one modified by epoxy carbon showed higher activity and stability. The combination of characterizations and density functional theory modeling demonstrated that the clean Pt on CeO2 rapidly deactivated due to the CO self-poisoning albeit high initial activity, and conversely, low initial activity was observed for the more stable graphite-covered catalyst due to the obstruction of the Pt site. In contrast, epoxy carbon species on Pt shifted the d-band of Pt to lower energy, weakening the Pt-CO binding strength. Such a modification mitigated the self-poisoning effect while maintaining ample active sites and enabling the complete oxidative removal of CO under ambient conditions. This work may provide a general approach to tackling the self-poisoning issue.
RESUMO
ETHNOPHARMACOLOGICAL RELEVANCE: Erjingpill, a well-known prescription documented in the classic Chinese medical text "Shengji Zonglu," has been proven to have effective alleviating effects on neuroinflammation in Alzheimer's disease (AD). Although the alterations in microglial cell glycolysis are known to play a crucial role in the development of neuroinflammation, it remains unclear whether the anti-neuroinflammatory effects of Erjingpill are associated with its impact on microglial cell glycolysis. AIM OF THE STUDY: This study aims to determine whether Erjingpill exerts anti-neuroinflammatory effects by influencing microglial cell glycolysis. MATERIALS AND METHODS: Firstly, Erjingpill decoction was prepared into an Erjingpill bionic cerebrospinal fluid (EBCF) through a process of in vitro intestinal absorption, hepatocyte incubation, and blood-brain barrier (BBB) transcytosis. Subsequently, UPLC/Q-TOF-MS/MS technology was used to analyze the compounds in Erjingpill and EBCF. Next, an in vitro neuroinflammation model was established by LPS-induced BV2 cells. The impact of EBCF on BV2 cell proliferation activity was evaluated using the CCK-8 assay, while the NO release was assessed using the Griess assay. Additionally, mRNA levels of pro-inflammatory factors (IL-1ß, IL-6, TNF-α, and COX-2), anti-inflammatory factors (IL-10, IL-4, Arg-1, and TGF-ß), M1 microglial markers (iNOS, CD86), M2 microglial markers (CD36, CD206), and glycolytic enzymes (HK2, GLUT1, PKM, and LDHA) were measured using qPCR. Furthermore, protein expression of microglial activation marker Iba-1, M1 marker iNOS, and M2 marker CD206 were identified through immunofluorescence, while concentrations of pro-inflammatory cytokines IL-1ß and TNF-α were measured using ELISA. Enzymatic activity of glycolytic enzymes (HK, PK, and LDH) was assessed using assay kits, and the protein levels of pro-inflammatory factors (IL-1ß, iNOS, and COX-2), anti-inflammatory factors (IL-10 and Arg-1), and key glycolytic proteins GLUT1 and PI3K/AKT/mTOR were detected by Western blot. RESULTS: Through the analysis of Erjingpill and EBCF, 144 compounds were identified in Erjingpill and 40 compounds were identified in EBCF. The results demonstrated that EBCF effectively inhibited the elevation of inflammatory factors and glycolysis levels in LPS-induced BV2 cells, promoted polarization of M1 microglial cells towards the M2 phenotype, and suppressed the PI3K/AKT/mTOR inflammatory pathway. Moreover, EBCF alleviated LPS-induced BV2 cell inflammatory response by modulating mTOR to inhibit glycolysis. CONCLUSIONS: EBCF exhibits significant anti-neuroinflammatory effects, likely attributed to its modulation of mTOR to inhibit microglial cell glycolysis. This study furnishes experimental evidence supporting the clinical utilization of Erjingpill for preventing and treating AD.