Potential of queen bee larvae as a dietary supplement for obesity management: modulating the gut microbiota and promoting liver lipid metabolismLi, Chen, Shi
et alFood Funct (2025)
Abstract: Queen bee larvae (QBL) have been consumed as both a traditional food and medicine in China for thousands of years; however, their specific benefits for human health, particularly their potential anti-obesity property, remain underexplored. This study investigated the anti-obesity effect of QBL freeze-dried powder (QBLF) on high-fat diet (HFD) induced obesity in mice and explored the underlying mechanisms. Our findings showed that QBLF effectively reduced body weight, fasting blood glucose levels, lipid accumulation, and inflammation in HFD mice. 16S rRNA sequencing revealed that QBLF significantly modulated the gut microbiota disrupted by an HFD, notably increasing the relative abundance of beneficial microbes such as Ileibacterium, Clostridium sensu stricto 1, Incertae sedis, Streptococcus, Lactococcus, Clostridia UCG-014, and Lachnospiraceae UCG-006, which were inversely associated with obesity-related phenotypes in the mice. RNA sequencing analysis further demonstrated that QBLF intervention upregulated the expression of genes involved in liver lipid metabolism, including Pck1, Cyp4a10, Cyp4a14, and G6pc, while downregulating genes associated with the inflammatory response, such as Cxcl10, Ccl2, Traf1, Mapk15, Lcn2, and Fosb. These results suggested that QBLF can ameliorate HFD-induced obesity through regulating the gut microbiota, promoting liver lipid metabolism, and reducing inflammatory response.
Melatonin Alleviates Behavioral and Neurodevelopmental Abnormalities in Offspring Caused by Prenatal StressWu, Du, Zhao
et alCNS Neurosci Ther (2025) 31 (3), e70347
Abstract: Prenatal stress (PNS) is a significant risk factor impacting the lifelong health of offspring, and it has been widely recognized as being closely linked to the increased prevalence of neurodevelopmental disorders and psychiatric illnesses. However, effective pharmacological interventions to mitigate its detrimental effects remain limited. Melatonin (Mel), an endogenous hormone, has demonstrated considerable potential in treating neurological diseases due to its anti-inflammatory, antioxidant, and neuroprotective properties, as well as its favorable safety profile and broad clinical applicability.This study aims to investigate the protective effects and mechanisms of melatonin on neurodevelopmental and behavioral abnormalities in offspring induced by prenatal stress.Using a prenatal stress mouse model, we evaluated the effects of melatonin on emotional and cognitive deficits in offspring. Neurogenesis and synaptic development were assessed, and RNA sequencing was performed to analyze microglial gene enrichment and immune-related pathways. Both in vivo and in vitro experiments were conducted to validate the findings, focusing on the PI3K/AKT/NF-κB signaling pathway in microglia.Melatonin administration alleviated emotional and cognitive deficits in offspring mice exposed to prenatal stress, addressing abnormalities in neurogenesis and synaptic development. Additionally, RNA sequencing revealed that melatonin suppresses microglial gene enrichment and the upregulation of immune-related pathways. Both in vivo and in vitro validation indicated that melatonin modulates the PI3K/AKT/NF-κB signaling pathway in microglia, reducing the elevated expression of CXCL10 in the dentate gyrus, thereby restoring normal neuro-supportive functions and optimizing the neurodevelopmental environment.These findings suggest that melatonin significantly improves neurodevelopmental disorders and behavioral abnormalities caused by prenatal stress by inhibiting pathological microglial activation and promoting hippocampal neurogenesis and synaptic plasticity. This provides new insights into melatonin's potential as a neuroprotective agent for treating prenatal stress-related disorders.© 2025 The Author(s). CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.
Identification and validation of prognostic biomarkers related to tumor immune invasion in pancreatic cancerChen, Zhou, Fan
et alFront Genet (2025) 16, 1556544
Abstract: The diagnosis and treatment of pancreatic adenocarcinoma (PAAD) remain clinically challenging, and new molecular markers for prognostic assessment and targeted therapy are urgently needed. The tumor microenvironment (TME) and immune invasion play an important role in pancreatic cancer development and progression. Therefore, immunotherapeutic strategies based on the TME and immune invasion may have important clinical value.In this study, we extracted transcriptome and clinicopathological data for 179 PAAD samples from the TCGA database and evaluated the immune composition, stromal composition, and infiltrating immune cell landscape in the tumor samples. Then, we identified relevant differentially expressed genes (DEGs) and performed functional annotation and prognostic correlation analysis to identify prognostic biomarkers for pancreatic cancer, the correlation between biomarkers and tumor immune invasion was analyzed to reveal the molecular immune mechanism of pancreatic cancer. Finally, GEO databases (GES71729), GEPIA, TISIDB, TIMER databases and RT-PCR were used for further analysis.CXCL10 and CXCL11 were highly expressed in pancreatic cancer and associated with poor prognosis of patients through cell adhesion molecules chemokine signaling, cytokine-cytokine receptor interaction, natural killer cell-mediated cytotoxicity, and Toll-like receptor signaling pathways. Finally, the correlation between CXCL10 and CXCL11 and tumor immune invasion was analyzed. The results confirmed that the expression levels of CXCL10 and CXCL11 were positively correlated with the contents of CD8+ T cells. Activated memory CD4+ T cells, M1 macrophages and resting mast cells. The levels of CXCL10 and CXCL11 were related to but negatively correlated with the contents of memory B cells, Tregs and M0 macrophages.Our study demonstrates that CXCL10 and CXCL11 are novel biomarkers of TME and immune cell infiltration in pancreatic cancer by affecting the distribution of immune cells. CXCL10 and CXCL11 may be new targets for molecular targeted therapy and immunotherapy of pancreatic cancer.Copyright © 2025 Chen, Zhou, Fan and Wang.
Unveiling the role of CXCL10 in pancreatic cancer progression: A novel prognostic indicatorWu, Rong, Tang
et alOpen Med (Wars) (2025) 20 (1), 20241117
Abstract: Pancreatic cancer is distinguished by its high likelihood of metastasis and drug resistance, while the fundamental mechanisms are inadequately elucidated. This study aimed to identify pivotal hub genes associated with pancreatic cancer and assess their potential utility in predicting its onset and progression.Weighted gene co-expression network analysis (WGCNA) combined with differential expression analysis identified novel susceptibility modules and hub genes for pancreatic cancer. Kyoto Encyclopedia of Genes and Genomes and gene ontology analyses were utilized to explore the potential roles of these hub genes. Receiver operator characteristic curves and nomogram models were developed to evaluate diagnostic efficacy. Mendelian randomization, flow cytometry, Transwell, and RNA sequencing were conducted to explore the association between C-X-C motif chemokine ligand 10 (CXCL10) and immune infiltration.WGCNA analysis was performed to build gene co-expression networks, and ten key genes were found. CXCL10 was the central gene, and its expression was significantly linked to the survival of patients with pancreatic cancer and their response to immune checkpoint inhibitors. CXCL10 demonstrated the ability to stimulate the differentiation of macrophages toward the M2 phenotype. CXCL10 could facilitate the metastasis of pancreatic cancer cells by modulating macrophage polarization. CXCL10 affects macrophage polarization by regulating the expression of vascular endothelial growth factor A.CXCL10 demonstrates potential as a therapeutic target for managing pancreatic cancer.© 2025 the author(s), published by De Gruyter.
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