We aimed to know the effect of nuclear factor‐kappa B (NF‐κB) inhibition on the kidney injury of systemic lupus erythematosus (SLE) mice. Pristane‐induced SLE mice were treated with pyrrolidine dithiocarbamate (PDTC, 50 or 100 mg/kg), a NF‐κB inhibitor. Histopathological changes were observed by hematoxylin & eosin, Masson and periodic schiff‐methenamine stainings. Long noncoding RNA Taurine upregulated gene 1 (LncRNA TUG1) was measured by real‐time reverse transcription PCR, NF‐κB p65 expression by western blotting, levels of inflammatory cytokines, antinuclear antibodies (ANA), and antidouble stranded DNA (anti‐dsDNA) by enzyme‐linked immunosorbent assay, and the deposition of IgG and C3 by immunofluorescence. The kidney of SLE mice exhibited interstitial inflammatory cell infiltration, interstitial fibrous proliferation, glomerular mesangial proliferation, and crescent formation, which was mitigated after PDTC administration. The levels of BUN, Cr, ANA, and anti‐dsDNA and the pro‐inflammatory factors in SLE mice were increased with obvious deposition of IgG and C3, but they were also reversed by PDTC. Furthermore, the NF‐κB p65 expression in the nucleus in the SLE mice was decreased with the up‐regulation of TUG1 expression and NF‐κB p65 expression in the cytoplasm after PDTC treatment. Correlation analysis revealed the negative correlation between the TUG1 expression and NF‐κB p65 in the nucleus in the kidney tissues. NF‐κB inhibition with PDTC protected against the kidney injury of pristine‐induced SLE mice possibly via up‐regulating lncRNA TUG1, and further clinical studies are needed to clarify whether NF‐κB inhibition may be a therapeutic modality for the kidney injury of SLE.

Monolayer transition‐metal dichalcogenides, e.g., MoS 2 , typically have high intrinsic strength and Young's modulus, but low fracture toughness. Under high stress, brittle fracture occurs followed by cleavage along a preferential lattice direction, leading to catastrophic failure. Defects have been reported to modulate the fracture behavior, but pertinent atomic mechanism still remains elusive. Here, sulfur (S) and MoS n point defects are selectively created in monolayer MoS 2 using helium‐ and gallium‐ion‐beam lithography, both of which reduce the stiffness of the monolayer, but enhance its fracture toughness. By monitoring the atomic structure of the cracks before and after the loading fracture, distinct atomic structures of the cracks and fracture behaviors are found in the two types of defect‐containing monolayer MoS 2 . Combined with molecular dynamics simulations, the key role of individual S and MoS n point defects is identified in the fracture process and the origin of the enhanced fracture toughness is elucidated. It is a synergistic effect of defect‐induced deflection and bifurcation of cracks that enhance the energy release rate, and the formation of widen crack tip when fusing with point defects that prevents the crack propagation. The findings of this study provide insights into defect engineering and flexible device applications of monolayer MoS 2 .