Isoliquiritigenin (ILQ) has a number of biological activities such as antitumor and anti-inflammatory effects. However, biomedical applications of ILQ are impeded by its poor aqueous solubility. Therefore, in this research, we prepared a novel ILQ-loaded nanoemulsion, i.e., ILQ-NE, which consisted of Labrafil^® M 1944 CS (oil), Cremophor^® EL (surfactant), ILQ, and phosphate-buffered saline, by employing a combined sonication (high-energy) and phase-inversion composition (low-energy) method (denoted as the SPIC method). The ILQ-NE increased the ILQ solubility ~1000 times more than its intrinsic solubility. It contained spherical droplets with a mean diameter of 44.10 ± 0.28 nm and a narrow size distribution. The ILQ loading capacity was 4%. The droplet size of ILQ-NE remained unchanged during storage at 4 °C for 56 days. Nanoemulsion encapsulation effectively prevented ILQ from degradation under ultraviolet light irradiation, and enhanced the ILQ in vitro release rate. In addition, ILQ-NE showed higher cellular uptake and superior cytotoxicity to 4T1 cancer cells compared with free ILQ formulations. In conclusion, ILQ-NE may facilitate the biomedical application of ILQ, and the SPIC method presents an attractive avenue for bridging the merits and eliminating the shortcomings of traditional high-energy methods and low-energy methods.

Exposure to Aflatoxin B1 (AFB1) is considered a significant risk factor for human diseases, including the immune function impairment of immune cells. Dendritic cells (DCs), as essential antigen-presenting cells, play a pivotal role in bridging innate and adaptive immunity. However, the impact of AFB1 exposure on DCs has not been fully elucidated. In this study, we investigated the effects of AFB1 exposure on the migration ability of DCs and its underlying action model. Initially, we observed that AFB1 exposure inhibited the survival of DCs and altered their cellular morphology. Further investigation revealed that AFB1 promotes cell adhesion and inhibits DC migration by modulating the expression of cell adhesion molecules. Additionally, our findings indicated that cytoskeletal remodeling plays a crucial role in these processes. Experimental techniques such as immunofluorescence and RNA sequencing confirmed that AFB1 exposure regulates the expression of cytoskeleton-related genes. Moreover, we found that the perturbation of the gene expression profile through AFB1 exposure is associated with cell communication. Collectively, our study findings demonstrate that AFB1 can disrupt the expression of cytoskeleton- and adhesion-related molecules in DCs, thereby altering cell morphology and migration. These insights could provide new perspectives for further understanding the immunosuppressive effects of AFB1 and developing therapeutic strategies for diseases associated with AFB1 exposure.

Introduction: The effective and persistent suppression of hepatitis B surface antigen (HBsAg) in patients with chronic HBV infection (CHB) is considered to be a promising approach to achieve a functional cure of hepatitis B. In our previous study, we found that the antibody E6F6 can clear HBsAg through FcγR-mediated phagocytosis, and its humanized form (huE6F6 antibody) is expected to be a new tool for the treatment of CHB. Previous studies have shown that the glycosylation of Fc segments affects the binding of antibodies to FcγR and thus affects the biological activity of antibodies in vivo.Methods: To further improve the therapeutic potential of huE6F6, in this study, we defucosylated huE6F6 (huE6F6-fuc-), preliminarily explored the developability of this molecule, and studied the therapeutic potential of this molecule and its underlying mechanism in vitro and in vivo models.Results: huE6F6-fuc- has desirable physicochemical properties. Compared with huE6F6-wt, huE6F6-fuc- administration resulted in a stronger viral clearance in vivo. Meanwhile, huE6F6-fuc- keep a similar neutralization activity and binding activity to huE6F6-wt in vitro. Immunological analyses suggested that huE6F6-fuc- exhibited enhanced binding to hCD32b and hCD16b, which mainly contributed to its enhanced therapeutic activity in vivo.Conclusions: In summary, the huE6F6-fuc- molecule that was developed in this study, which has desirable developability, can clear HBsAg more efficiently in vivo, providing a promising treatment for CHB patients. Our study provides new guidance for antibody engineering in other disease fields.