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MXenes are promising cathode materials for aqueous zinc-ion batteries (AZIBs) owing to their layered structure, metallic conductivity, and hydrophilicity. However, they suffer from low capacities unless they are subjected to electrochemically induced second phase formation, which is tedious, time-consuming, and uncontrollable. Here we propose a facile one-step surface selenization strategy for realizing advanced MXene-based nanohybrids. Through the selenization process, the surface metal atoms of MXenes are converted to transition metal selenides (TMSes) exhibiting high capacity and excellent structural stability, whereas the inner layers of MXenes are purposely retained. This strategy is applicable to various MXenes, as demonstrated by the successful construction of VSe2@V2CT x , TiSe2@Ti3C2T x , and NbSe2@Nb2CT x . Typically, VSe2@V2CT x delivers high-rate capability (132.7 mA h g–1 at 2.0 A g–1), long-term cyclability (93.1% capacity retention after 600 cycles at 2.0 A g–1), and high capacitive contribution (85.7% at 2.0 mV s–1). Detailed experimental and simulation results reveal that the superior Zn-ion storage is attributed to the engaging integration of V2CT x and VSe2, which not only significantly improves the Zn-ion diffusion coefficient from 4.3 × 10–15 to 3.7 × 10–13 cm2 s–1 but also provides sufficient structural stability for long-term cycling. This study offers a facile approach for the development of high-performance MXene-based materials for advanced aqueous metal-ion batteries.

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Secretion of proinflammatory cytokines by LPS activated endothelial cells contributes substantially to the pathogenesis of sepsis. However, the mechanism involved in this process is not well understood. In the present study, we determined the roles of GEF-H1 (guanine-nucleotide exchange factor-H1)-RhoA signaling in LPS-induced interleukin-8 (IL-8, CXCL8) production in endothelial cells. First, we observed that GEF-H1 expression was upregulated in a dose- and time-dependent manner as consistent with TLR4 (Toll-like receptor 4) expression after LPS stimulation. Afterwards, Clostridium difficile toxin B-10463 (TcdB-10463), an inhibitor of Rho activities, reduced LPS-induced NF-κB phosphorylation. Inhibition of GEF-H1 and RhoA expression reduced LPS-induced NF-κB and p38 phosphorylation. TLR4 knockout blocked LPS-induced activity of RhoA, however, MyD88 knockout did not impair the LPS-induced activity of RhoA. Nevertheless, TLR4 and MyD88 knockout both significantly inhibited transactivation of NF-κB. GEF-H1-RhoA and MyD88 both induced significant changes in NF-κB transactivation and IL-8 synthesis. Co-inhibition of GEF-H1-RhoA and p38 expression produced similar inhibitory effects on LPS-induced NF-κB transactivation and IL-8 synthesis as inhibition of p38 expression alone, thus confirming that activation of p38 was essential for the GEF-H1-RhoA signaling pathway to induce NF-κB transactivation and IL-8 synthesis. Taken together, these results demonstrate that LPS-induced NF-κB activation and IL-8 synthesis in endothelial cells are regulated by the MyD88 pathway and GEF-H1-RhoA pathway.