Hyperuricemia, a metabolic disorder marked by dysregulated uric acid (UA) metabolism, significantly contributes to the development of various chronic diseases. The homeostatic control of UA, affected by genetic background, environmental cues, and gut microbial activity, is essential for preventing dysregulated serum UA levels. Evidence indicates that high-purine diets cause gut dysbiosis and increase intestinal permeability, enabling translocation of harmful metabolites into systemic circulation. This can provoke renal inflammation and impair UA excretion, exacerbating hyperuricemia (HUA). The gut and kidneys interact bidirectionally through the gut-kidney axis, which is influenced by gut microbiota and their metabolites. Probiotics have demonstrated potential in restoring gut-kidney axis function and modulating UA metabolism by regulating the levels of short-chain fatty acids, bile acids, proline, and tryptophan derivatives. Nonetheless, comprehensive reviews on probiotic interventions for hyperuricemia remain scarce. This review explores the intricate interplay among gut-kidney axis, gut microbiota and metabolites, UA metabolism, and HUA. It further outlines the role of probiotics in regulating gut microbiota and UA metabolism. Finally, probiotic strategies including direct supplementation, functional foods, synbiotics, and delivery systems are summarized for the management of HUA. Despite this promise, challenges in strain selection, dosage standardization, and industrial scalability must be addressed. Future research should aim to improve the stability of probiotic formulations and develop personalized microbiota interventions based on individual variables.

As a frontline chemotherapeutic agent, cyclophosphamide (CTX) frequently induces severe treatment-related adverse effects. Probiotics have emerged as promising dietary adjuvants to alleviate chemotherapy-induced toxicity. This study aimed to explore the alleviate mechanism of Lactobacillus plantarum Lp2 isolated from a traditional fermented food on CTX-induced splenic and intestinal injuries. In CTX-induced mice, oral Lp2 concurrently activated the TLR2/NF-κB/NLRP3 and Nrf2/HO-1 signaling pathways in the spleen, thereby enhancing the levels of cytokines (IL-2, IL-6, IL-1β, TNF-α, and IFN-γ) and the activity of antioxidant enzymes (CAT, SOD, and GSH), protecting splenic architecture and function. Intestinal NLRP3 inflammasome activation by Lp2 modulated similar cytokine profiles (IL-2, IL-6, IL-1β, TNF-α, IFN-γ), demonstrating its gut- immunoregulatory capacity in CTX-induced mice. Furthermore, Lp2 enhanced short-chain fatty acid (SCFA) metabolism and intestinal barrier by modulating the gut microbiota composition through specific bacterial populations, including Clostridium, Duncaniella, Alistipes, Muribaculum, among others, thereby sustaining intestinal physiological homeostasis. These findings established Lp2 as a multifunctional probiotic capable of mitigating CTX chemotherapy-associated side effects, providing a theoretical basis for the development of probiotic dietary supplements.

In this study, the metabolic mechanism underlying the efficient accumulation of astaxanthin in Phaffia rhodozyma PR106 induced by titanium dioxide (TiO₂) stress was investigated by the combined use of untargeted metabolomics and microscopic observation. Metabolomic analysis revealed that TiO₂ stress significantly changed intracellular metabolites closely linked to astaxanthin biosynthesis in PR106 cells, such as sucrose, 5-dehydroepisterol, and (6Z)-octadecenoic acid, which were downregulated after 16 h and upregulated after 32 h. Furthermore, TiO₂ stress promoted astaxanthin synthesis by regulating key metabolic pathways, including ABC transporters, the phosphotransferase system, steroid biosynthesis, and amino acid biosynthesis, which were highly consistent with the major metabolic pathway changes observed during astaxanthin accumulation in PR106. In addition, TiO₂ stress reduced cell wall permeability, enhanced membrane fluidity, and increased the number of lipid droplets and mitochondria. This study provides a theoretical basis for rational redesign of P. rhodozyma based on the metabolic mechanism to enhance astaxanthin accumulation, thus helping to achieve efficient astaxanthin production by P. rhodozyma.

Alcohol-related liver injury is a widespread global health concern caused by chronic excessive alcohol consumption, with inflammation serving as the central mechanism driving disease progression. Although contemporary medical interventions offer diverse therapeutic options for alcohol-related liver disease (ALD), their efficacy is limited and may induce undesirable adverse effects. Probiotics, prebiotics, synbiotics, and postbiotics have emerged as promising therapeutic strategies due to their food-grade safety and anti-inflammatory properties. To date, there remains a lack of a comprehensive review on the impact of these biotic interventions on alcohol-related liver injury. This review examines how the metabolic byproducts generated during alcohol metabolism trigger inflammatory responses and explores the potential mechanisms linking inflammation to the progression of ALD. It also highlights that probiotics, prebiotics, synbiotics, and postbiotics represent promising therapeutic strategies due to their food-grade safety and anti-inflammatory properties.

Lactiplantibacillus plantarum 104, which was previously screened in the laboratory, has been confirmed to have the effect of lowering lipids and regulating intestinal microbial homeostasis. However, the mechanism of action of its fermentation supernatant in alleviating metabolic disorders is unclear. L. plantarum 104 cell-free supernatant (LP104s) was fed to high-fat diet C57BL/6N mice for 8 weeks. The intervention of LP104s increased the concentration of conjugated bile acids in the ileum, especially taur-α/β-muricholic acid sodium salt (T-α-MCA or T-β-MCA), inhibited intestinal farnesoid X receptor (FXR) -related signaling pathways. LP104s reduced cholesterol levels by increasing the synthesis of hepatic cholic acid (CA), chenodeoxycholic acid (CDCA), and the excretion of bile acids in feces. Moreover, Western blotting results showed that TLR2/NF-κB signaling pathway expression was inhibited. In addition, 16S rRNA sequencing results showed that LP104s regulated the relative abundance of bacteria associated with inflammatory response and obesity (Prevotella, Ruminococcus, and Clostridium). Therefore, this paper further elaborates the role of gut microbiology and bile acids in improving metabolism from the perspective of secondary bile acids and intestinal chronic inflammation and also lays a theoretical foundation for the next step in the development of fermentation products of this strain.

The gut microbiota and it’s metabolism are vital targets of probiotics regulating high fat-diet (HFD) induced hyperlipidemia, which can relieve the pressure caused by the striking growth of sub-health people. Pediococcus pentosaceus PP04 (PP04) could colonize in intestine to regulate gut microbiota and it’s metabolites directly, the rebalanced intestinal flora mediated by PP04 could facilitate the secretion of short chain fatty acids to control body weight gain, PP04 intervention also changed bile acid (BA) profiles and enhanced the ileal concentrations of antagonists including tauro-α/β-muricholic acid sodium salt and ursodeoxycholic acid to inhibit intestinal farnesoid X receptor/fibroblast growth factor 15 (FXR/FGF15) signaling coupled with the activation of hepatic FXR/small heterodimer partners signaling, which accelerated the hepatic BA de novo synthesis and excretion with feces to eliminate HFD caused hyperlipemia effectively. This study provided important evidence regarding PP04 as dietary supplement to relieve hyperlipidemia by influencing BA enterohepatic circulation.

This study aimed to investigate the effect of ginseng glucosyl oleanolate (GGO) on non-small cell lung cancer (NSCLC) both in vitro and in vitro. GGO significantly inhibited the proliferation of A549 cells and tumor growth of A549-xenograft nude mice. Metabonomics analysis showed that GGO treatment changed the metabolites of glycolysis and TCA cycle, which was consistent with KEGG enrichment analysis of transcriptomics. GGO inhibited the expression of glutaminase (GLS), decreased the content of glutamic acid and the carbon input of the TCA cycle, and finally significantly blocked the production of ATP. Meanwhile, GGO treatment decreased the levels of glutathione (GSH) and glutathione peroxidase (GSH-PX), increased the accumulation of Fe²⁺ and malondialdehyde (MDA), downregulated solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4) protein expression, which led to the redox imbalance and induced ferroptosis in A549 cells and tumor tissue. These findings provided compelling evidence that GGO may represent a potential new approach to treating NSCLC.

Trehalose (TRE) was used to improve the gastrointestinal tolerance of Lactobacillus plantarum embedded with whey protein concentrate/pullulan (WPC/PUL) hydrogel and the embedded L. plantarum was applied to juice. The study indicated that 5% TRE significantly increased the viable counts of L. plantarum embedded in WPC/PUL hydrogel from (8.83 ± 0.03) to (9.14 ± 0.04) (lg (CFU/g)) in simulated gastric juice (SGJ) and from (9.13 ± 0.04) to (9.38 ± 0.04) (lg (CFU/g)) in simulated intestinal juice, respectively. The addition of TRE improved the glass transition temperature of WPC/PUL hydrogel and decreased the hardness and its solubility in SGJ, which may be responsible for the improved protection of WPC/PUL hydrogels on L. plantarum. In addition, TRE increased the viable counts of L. plantarum in WPC/PUL probiotic microcapsule juice at low pH and high temperature during storage.