Objective To investigate the role of curcumin in the treatment of lupus nephritis (LN) by inhibiting the migration of neutrophils and the underlying mechanism involved. Methods Two lupus mouse models, MRL/lpr mice and R848-treated mice, were treated with 50 mg/kg curcumin by intraperitoneal injection. H&E and Masson staining were used to estimate histopathological changes in the kidney. Immunofluorescence was used to assess the deposition of immune complexes. The expression of inflammatory factors was detected by enzyme-linked immunosorbent assay (ELISA) and real-time reverse transcription polymerase reaction (RT-PCR), and the protein expression was detected by western blotting. Results We revealed the remarkable potential of curcumin in improving inflammatory conditions in both MRL/lpr mice and R848-induced lupus mice. Curcumin effectively decelerates the progression of inflammation and diminishes the infiltration of neutrophils and their release of pivotal inflammatory factors, thereby reducing inflammation in renal tissues. Mechanistically, curcumin significantly inhibits the expression of p-PI3K, p-AKT and p-NF-κB, which are upregulated by interleukin-8 to induce neutrophil migration and renal inflammation, thereby reducing neutrophil migration and the release of inflammatory factors. Conclusion Curcumin significantly inhibits the recruitment of neutrophils and the release of proinflammatory factors in the kidney by inhibiting the PI3K/AKT/NF-κB signalling pathway, providing new therapeutic targets and medication strategies for the treatment of LN.

Mixed human umbilical cord‐derived mesenchymal stem cells (UC‐MSCs) are widely applied in clinical trials to treat various diseases due to their multipotent differentiation potential and immune regulatory activities. However, the lack of a clear understanding of their heterogeneity hampers their application to precisely treat diseases. Moreover, few studies have experimentally authenticated the functions of so‐called UC‐MSC subpopulations classified from scRNA‐seq samples. Here, this work draws a large‐scale single‐cell transcriptomic atlas and identified three clusters (C1, C2, and C3), representing the primed, intermediate, and stem statuses individually. The C1 and C3 clusters feature higher expression of cytokines and stemness markers, respectively. Surprisingly, further experimental assays reveal that the BAMBI^highMFGE8^high C1 subgroup has a unique phenotype, distinct transcriptomic profile, and limited adipogenic differentiation potential but compromised immunosuppressive activity in vitro and in vivo in lupus mice. Thus, this work is helpful to clarify the nature of human UC‐MSCs and to choose optimal MSC types to treat specific diseases in the future.

Mesenchymal stem cells (MSCs) are stem/progenitor cells capable of self-renewal and differentiation into osteoblasts, chondrocytes and adipocytes. The transformation of multipotent MSCs to adipocytes mainly involves two subsequent steps from MSCs to preadipocytes and further preadipocytes into adipocytes, in which the process MSCs are precisely controlled to commit to the adipogenic lineage and then mature into adipocytes. Previous studies have shown that the master transcription factors C/enhancer-binding protein alpha and peroxisome proliferation activator receptor gamma play vital roles in adipogenesis. However, the mechanism underlying the adipogenic differentiation of MSCs is not fully understood. Here, the current knowledge of adipogenic differentiation in MSCs is reviewed, focusing on signaling pathways, noncoding RNAs and epigenetic effects on DNA methylation and acetylation during MSC differentiation. Finally, the relationship between maladipogenic differentiation and diseases is briefly discussed. We hope that this review can broaden and deepen our understanding of how MSCs turn into adipocytes.

Background: Rheumatoid arthritis (RA) is a major public health problem. Unfortunately, there is a scarcity of comprehensive and up-to-date information regarding the burden of RA and its dynamic trends in subsequent years. To examine the changing trends in the global burden of RA and forecast for 2044, which will facilitate the development of strategies tailored to RA burden and provide reference for the development of effective treatment guidelines. Methods: Following the general analytical strategy used the Global Burden of Disease Study (GBD) 2019, which included 204 countries, the age-standardized incidence rate (ASIR), age-standardized mortality rate (ASMR) and age-standardized disability adjusted of life year (DALY) rate for RA were analyzed. Results: The ASIR, ASMR and age-standardized DALY rate for RA in 2019 were 13.001/100,000 (95% UI, 11.833 ~ 14.274), 0.574/100,000 (95% UI, 0.356 ~ 0.793) and 39.565/100,000 (95% UI, 49.529 ~ 30.508), respectively. America had the highest ASIR [18.578(95% UI, 17.147 ~ 20.148)] and age-standardized DALY rate [53.676(95% UI, 40.106 ~ 67.968)] in 2019. Asia had the highest ASMR [0.681(95% UI, 0.802 ~ 0.480)] in 2019. From 1990 to 2019, a significant average annual percentage change (AAPC) in the ASIR was observed in both males [0.237% (95% CI, 0.216 ~ 0.259%)] and females [0.197% (95% CI, 0.141 ~ 0.254%)], AAPC in the ASMR was observed in both males [-0.398% (95% CI, -0.605~-0.191%)] and females [-0.295% (95% CI, -0.424~-0.65%)]. Age effects indicated that the relative risk (RR) of RA-associated incidence and mortality rates increased with age among males and females. The RR of RA increased over time and started to gradually increase from 1990. Cohort effects showed decreases in incidence, mortality and DALY rates in successive birth cohorts. The global incidence of RA would continue to increase in the future, while mortality would continue to decrease. Conclusion: The increased risk of RA is dominantly influenced by age effects and period effects and the ethnic area. The results suggest that early identification and treatment of RA is important for reducing the ongoing burden with age, and targeted health education and specific intervention programs should be promoted to control middle-elderly population.

The positive CQD has good biocompatibility (≤800 μg mL⁻¹) and labelling performance for mesenchymal stem cell in vitro and in vivo.