The research progression of direct NLRP3 inhibitors to treat inflammatory disorders.

The NLRP3 inflammasome represents a cytoplasmic multiprotein complex with the capability to recognize a wide range of pathogen-derived, environmental, and endogenous stress-related factors. Dysregulated activation of the NLRP3 inflammasome has been implicated in the development of various inflammasome-associated disorders, highlighting its significance as a pivotal target for the treatment of inflammatory diseases. Nonetheless, despite its clinical importance, there is currently a lack of specific drugs available for directly targeting the NLRP3 inflammasome. Several strategies have been explored to target different facets of the NLRP3 inflammasome, with interventions aimed at directly inhibiting NLRP3 demonstrating the most promising efficacy and safety profiles. In this review, we provide a summary of direct inhibitors targeting NLRP3, elucidating their inhibitory mechanisms, clinical trial phases, and potential applications. Through this discussion, we aim to shed light on the implications of NLRP3 inhibition for the treatment of inflammatory diseases.

IGFBP2 drives epithelial-mesenchymal transition in hepatocellular carcinoma via activating the Wnt/ß-catenin pathway.

Metastasis has emerged as a major impediment to achieve successful therapeutic outcomes in hepatocellular carcinoma (HCC). Nonetheless, the intricate molecular mechanisms governing the progression of HCC remain elusive. Herein, we present evidence highlighting the influence exerted by insulin-like growth factor-binding protein 2 (IGFBP2) as a potent oncogene driving the malignant phenotype. Our investigation reveals a marked elevation of IGFBP2 expression in primary tumors, concomitant with the presence of mesenchymal biomarkers in HCC. Through in vitro and in vivo experimentation, we demonstrate that the overexpression of IGFBP2 expedites the progression of epithelial-mesenchymal transition (EMT) and facilitates the metastatic potential of HCC cells, chiefly mediated by the Wnt/ß-catenin signaling pathway. Notably, knockdown of IGFBP2 significantly decreased the expression of total and nuclear ß-catenin, N-cadherin and vimentin in the treatment of the specific activator of Wnt/ß-catenin CHIR-99021. Collectively, our findings identify IGFBP2 as a pivotal regulator within the HCC EMT axis, whereby its overexpression confers the distinctly aggressive clinical features characteristic of the disease.

A flexible plasma-treated silver-nanowire electrode for organic light-emitting devices.

Silver nanowires (AgNWs) are a promising candidate to replace indium tin oxide (ITO) as transparent electrode material. However, the loose contact at the junction of the AgNWs and residual surfactant polyvinylpyrrolidone (PVP) increase the sheet resistance of the AgNWs. In this paper, an argon (Ar) plasma treatment method is applied to pristine AgNWs to remove the PVP layer and enhance the contact between AgNWs. By adjusting the processing time, we obtained AgNWs with a sheet resistance of 7.2Ω/□ and a transmittance of 78% at 550 nm. To reduce the surface roughness of the AgNWs, a peel-off process was used to transfer the AgNWs to a flexible NOA63 substrate. Then, an OLED was fabricated with the plasma-treated AgNWs electrode as anode. The highest brightness (27000 cd/m2) and current efficiency (11.8 cd/A) was achieved with a 30 nm thick light emitting layer of tris-(8-hydroxyquinoline) aluminum doped with 1% 10-(2-benzothiazolyl)-2,3,6,7-tetrahydro-1,1,7,7-tetramethyl-1H,5 H,11H-(1)-benzopyropyrano(6,7-8-I,j)quinolizin-11-one. Compared to thermal annealing, the plasma-treated AgNW film has a lower sheet resistance, a shorter processing time, and a better hole-injection. Our results indicate that plasma treatment is an effective and efficient method to enhance the conductivity of AgNW films, and the plasma-treated AgNW electrode is suitable to manufacture flexible organic optoelectronic devices.