ABSTRACT
The rational optimization of the electromagnetic field enhancement and charge transfer in a Raman substrate is vital for achieving efficient surface-enhanced Raman scattering (SERS). Herein, a ternary plasmonic substrate, whose structure-adjustable Au nanotriangle/Cu2O hybrids are combined with two-dimensional Ti3C2Tx MXene ultrathin nanosheets, is prepared and used for efficient SERS detection of molecules. By controlling the growth of Cu2O on Au nanotriangles, Au/Cu2O hybrids with three tips exposed are prepared, which show much better SERS performance than bare Au and core-shell Au@Cu2O in detecting methylene blue (MB) under excitation at 785 nm due to the optimized electromagnetic field enhancement and charge transfer. Furthermore, the Au/Cu2O hybrids are transferred to the plasmonic Ti3C2Tx nanosheet, generating a further enhanced electromagnetic field around their interfaces. As a result, the MXene/Au/Cu2O hybrids present further improved SERS activity, and their analytical enhancement factor reaches 2.4 × 109 and the detection limit is as low as 10-12 M. The enhancement mechanism can be ascribed to the improved electric field enhancement around the Au tips and the interface between MXene and Au/Cu2O. Meanwhile, the multiple charge-transfer processes between Au, Cu2O, MXene, and MB also play an important role in improving the SERS signal.
ABSTRACT
BACKGROUND: Activation of the nuclear factor B (NF-κB) signaling pathway by pattern recognition receptors (PRRs) is regarded as a crucial mechanism of neuroinflammation and brain injury after acute ischemic stroke. The stimulation of alpha-kinase 1 (ALPK1), a newly identified PRR, triggers NF-κB activation and an inflammatory response. Longitudinal population-based genetic epidemiological studies suggest that the ALPK1 gene is a susceptible site to ischemic stroke. However, the function of ALPK1 in the central nervous system remains unclear. The present study explored the role of ALPK1 in acute ischemic stroke. METHODS: BV2 microglial cells were stimulated with conditioned medium (CM) that was collected from oxygen and glucose deprivation (OGD)-treated HT22 neurons, and a murine brain ischemia model was established to detect the changes of ALPK1 expression. We used lentivirus to knockdown ALPK1 to explore the effects of ALPK1 in cerebral ischemia models in vitro and in vivo. RESULTS: We observed a significant increase of ALPK1 expression in BV2 cells that were stimulated with OGD CM. The knockdown of ALPK1 inhibited the phosphorylation of tumor necrosis factor receptor associated factor-interacting protein with a forkhead-associated domain (TIFA), the expression of tumor necrosis factor receptor-associated factor 6 (TRAF6), the activation of NF-κB, and the levels of proinflammatory factors in the BV2 cells. We also verified a neuroprotective effect of ALPK1 knockdown against ischemic brain injury through inhibition of the TIFA/TRAF6/NF-κB pathway and neuroinflammation in mice. CONCLUSIONS: This study demonstrates that ALPK1 is implicated in sterile inflammatory injury after acute brain ischemia, which provides first evidence for the therapeutic potential of ALPK1 inhibition in ischemic stroke.
