Figure 6. The impact of V₂O₅ ENM on NLRP3 inflammasome activation by inhibiting membrane Na⁺/K⁺ ATPase.

(A) Membrane Na⁺/K⁺ ATPase activity in NPs-induced KUP5 cells. KUP5 cells, exposed to V₂O₅, SiO₂, TiO₂ NPs and V⁵⁺ ions, were sonicated to collect the lysed cell pellets in a centrifuge tube. The pellets were used to assess Na⁺/K⁺ ATPase activity with a commercial kit (MyBioSource). *p < 0.05 compared to control cells. (B) Cell viability. In response to treatment with V₂O₅ NPs and V⁵⁺ ions in KUP5 cells. An MTS assay was used to assess the viability of LPS-primed (1 μg/mL for 4 h) KUP5 cells that were subsequently exposed to V₂O₅ NPs and V⁵⁺ ions for 18 h. The viability of nontreated control cells was regarded as 100%. *p < 0.05 compared to control cells. (C) Intracellular K⁺ leakage in KUP5 cells. Same experiment as in Figure 5C, using KUP5 cells exposed to V₂O₅, SiO₂, TiO₂ NPs and V⁵⁺ ion. TiO₂ NPs were used as a negative control. Triton X-100 (0.2 %) was used as positive control. Data were expressed as % change in RFI, which is defined as the percentage change of fluorescence intensity of treated cells normalized to the intensity of non-treated control cells. *p < 0.05 compared to control cells. (D) Schematic to explain the mechanism of V₂O₅ NPs toxicity through their effect on interference in Na⁺/K⁺ ATPase activity, potassium efflux, NLRP3 inflammasome assembly and IL-1β release.