Cold-brewed jasmine tea (CB-JT) is regarded to possess characteristic flavors and health benefits as a novel resource of functional tea beverages. To investigate the molecular mechanisms underlying CB-JT-mediated protective effects on obesity, we evaluated the serum biochemistry, histological condition, glucose tolerance, gene expression profile and intestinal microbial diversity in high-fat diet (HFD)-fed mice. Our results demonstrate that cold-brewed jasmine tea can significantly attenuate HFD-induced body weight gain, abnormal serum lipid levels, fat deposition, hepatic injury, inflammatory processes as well as metabolic endotoxemia. CB-JT also modified the microbial community composition in HFD-fed mice and altered the balance to one closely resembled that of the control group. The differential abundance of core microbes in obese mice was reversed by CB-JT treatment, including an increment in the abundance of Blautia, Mucispirillum, and Bilophila as well as a decrease in the abundance of Alloprevotella. CB-JT was proved to regulate the mRNA expression levels of lipid metabolism-related genes such as Leptin, Pgc1a Il6, and Il1b in the adipose tissue coupled with Cyp7a1, Lxra, Srebp1c, and Atgl in the liver. These findings indicate that cold-brewed jasmine tea might be served as a potential functional tea beverage to prevent obesity and gut microbiota dysbiosis.

Probiotics exert beneficial effects on health improvement, infection prevention, and disease management. This study investigated the probiotic characteristics and safety parameters of Levilactobacillus brevis ZG2488, a novel strain isolated from healthy human feces. The strain exhibited robust tolerance to simulated gastrointestinal conditions, maintaining survival rates of 87.20% in artificial gastric juice (pH 3.0; 3 h) and 95.32% in 0.3% bile salt (24 h). Notably, L. brevis ZG2488 displayed superior microbial adhesion properties with high cell surface hydrophobicity (87.32%), auto-aggregation (81.15% at 24 h), and co-aggregation capacities with Escherichia coli ATCC 43895 (63.90%) and Salmonella typhimurium SL1344 (59.28%). Its adhesion to HT-29 cells (7.15%) surpassed that of the reference strain Lactobacillus rhamnosus GG (1.26%). Antimicrobial testing revealed broad-spectrum inhibitory effects against multidrug-resistant Klebsiella pneumoniae NK04152 and other pathogens. Comprehensive safety assessments confirmed the absence of hemolytic or DNase activity, along with appropriate antibiotic susceptibility to most antibiotics, except kanamycin, streptomycin, vancomycin, and penicillin G. Furthermore, L. brevis ZG2488 significantly enhanced nitric oxide production and upregulated the gene expression of nitric oxide synthase (iNOS) and proinflammatory cytokines (IL-1β, IL-6, and TNF-α) in RAW264.7 macrophages. These findings underscore L. brevis ZG2488 as a promising probiotic candidate with functionality in pathogen inhibition and immune modulation.

Influenza A virus (IAV) remains a major global threat, highlighting the need for host-targeted antiviral strategies. While some probiotics offer prophylactic protection, their therapeutic potential post-infection is poorly understood. Here, we investigated human-derived Lactobacillus brevis ZG2488 for its antiviral potential against IAV. Strikingly, a more pronounced reduction in viral titer was observed when live bacteria were administered therapeutically post-infection, compared to preventive pretreatment. Transcriptomic analysis suggested that the therapeutic effect of viable bacteria was associated with a modulated host response, including the downregulation of specific host factors implicated in viral replication (e.g., KPNA2, NUP98, EIF2S1) and a delayed interferon-beta (IFNB1) induction. In contrast, preventive effects appeared to be mediated by heat-stable components. These findings highlight a viability-dependent mode of action for L. brevis ZG2488 and contribute to the growing evidence that certain probiotics may exert antiviral effects through targeted host modulation rather than solely through broad immune activation.

Osteosarcoma primarily occurs in children and adolescents, and is a highly aggressive bone tumor, particularly presenting challenges in metastatic or recurrent cases due to chemoresistance. Emerging evidences suggest that histone deacetylase inhibitors (HDACis) may exert anti-tumor effects by enhancing the efficacy of various therapeutic modalities. However, the combination of traditional chemotherapy with HDACi-based treatment for osteosarcoma intervention has not been thoroughly explored. This study investigates the anticancer properties of HDACis and/or etoposide (VP16) on the osteosarcoma cell lines U2OS and SJSA-1. Cell viability, morphology, growth and apoptosis were evaluated after treatments, in addition to their influence on the expression levels of proteins associated with apoptotic processes. To elucidate the underlying mechanisms, we employed RNA sequencing, RT-qPCR, and Western blot analyses. Treatment with either HDACis or VP16 alone resulted in an antiproliferative effects in U2OS and SJSA-1 cell lines. Notably, HDACis significantly increased the sensitivity of osteosarcoma cells to VP16, as evidenced by marked differences in cell viability, growth, morphology and apoptosis. Furthermore, when compared to doxorubicin treatment, this VP16/TSA/NAM combinatory regimen demonstrated a comparable ability to suppress cell viability while exhibiting a more pronounced inhibition of cell proliferation. Mechanistically, the combination of HDACis and VP16 specifically resulted in inhibition of the Hippo/YAP signaling cascade, accompanied by a reduction in total YAP1 protein expression. Collectively, our findings suggest that HDACis potentiate the capacity of VP16 to hinder cellular proliferation and trigger apoptosis via the downregulation of the Hippo/YAP pathway, thereby providing a prospective approach to overcome chemoresistance in osteosarcoma.