Oxidative stress, caused by the accumulation of reactive species, is associated with the initiation and progress of inflammatory bowel disease (IBD). The investigation of antioxidants to target overexpressed reactive species and modulate oxidant stress pathways becomes an important therapeutic option. Nowadays, antioxidative nanotechnology has emerged as a novel strategy. The nanocarriers have shown many advantages in comparison with conventional antioxidants, owing to their on-site accumulation, stability of antioxidants, and most importantly, intrinsic multiple reactive species scavenging or catalyzing properties. This review concludes an up-to-date summary of IBD nanomedicines according to the classification of the delivered antioxidants. Moreover, the concerns and future perspectives in this study field are also discussed.

Aging negatively affects B cell production, resulting in a decrease in B-1 and B-2 cells and impaired antibody responses. Age-related B cell subsets contribute to inflammation. Investigating age-related alterations in the B-cell pool and developing targeted therapies are crucial for combating autoimmune diseases in the elderly. Additionally, optimal nutrition, including carbohydrates, amino acids, vitamins, and especially lipids, play a vital role in supporting immune function and mitigating the age-related decline in B cell activity. Research on the influence of lipids on B cells shows promise for improving autoimmune diseases. Understanding the aging B-cell pool and considering nutritional interventions can inform strategies for promoting healthy aging and reducing the age-related disease burden.

Oxidative stress is closely linked to aging. Probiotics, whether viable or heat-inactivated, have shown antioxidant properties; however, their effect and mechanism of action in reducing oxidative stress during aging remains underexplored. This study examined the effects of viable and heat-inactivated Lactiplantibacillus plantarum TY-Y10 (L. plantarum TY-Y10) on D-galactose (D-gal)-induced aging in mice, aiming to uncover potential anti-aging mechanisms. Mice were induced to age with D-gal injections, then treated with sodium ascorbate (positive control) or varying doses of L. plantarum TY-Y10 for eight weeks. After treatment, oxidative stress markers, gut microbiota, and liver health were analyzed. Results showed that L. plantarum TY-Y10 decreased malondialdehyde (MDA) and inflammatory markers while increasing antioxidant levels (glutathione, superoxide dismutase, catalase and glutathione peroxidase). Liver damage was reduced, and expression of Nrf2 and related antioxidant enzymes improved. Additionally, L. plantarum TY-Y10 enhanced the abundance of short-chain fatty acid-producing bacteria, boosting fecal short-chain fatty acid levels. In short, both viable and heat-inactivated L. plantarum TY-Y10 mitigated oxidative stress in aging mice by modulating gut microbiota and activating liver antioxidant pathways through the gut-liver axis.

Given the limitations of clinical and potent natural α-glucosidase inhibitors, novel selective inhibitors are urgently needed. To accelerate discovery, we employed machine learning-integrated virtual screening to rapidly evaluate a library of 100 K⁺ compounds, identifying a series of selective α-glucosidase inhibitors. Activity validation demonstrated that these inhibitors exhibit significantly enhanced selectivity and potency compared to the positive control acarbose. Mechanistic studies through inhibition kinetics and fluorescence quenching revealed their improved inhibitory profile. Molecular docking indicates that key interactions—hydrogen bonding or salt bridges with the catalytic residue ASP526—strengthen binding within the active site. These interactions competitively obstruct enzyme-substrate binding, thereby amplifying inhibition. In vitro and in vivo starch digestion assays further corroborated these findings.

Selective inhibition of intestinal α‐glucosidase is an established strategy for controlling postprandial hyperglycemia. However, currently available inhibitors are predominantly reversible and nonselective, leading to incomplete target engagement, concomitant α‐amylase inhibition, and gastrointestinal side effects associated with gut microbiota perturbation. Here, we report a SuFEx‐enabled reprogramming strategy that converts natural flavonoids into highly selective α‐glucosidase covalent inhibitors. Guided by the structure of human intestinal maltase–glucoamylase, fluorosulfate warheads were introduced via Sulfur(VI) Fluoride Exchange (SuFEx) click chemistry, yielding covalently active derivatives with markedly enhanced affinity and selectivity toward α‐glucosidase over α‐amylase. The lead compound FS6‐2 forms an active‐site‐directed covalent interaction with a conserved lysine residue, resulting in sustained inhibition of starch digestion in vitro and in vivo. In diabetic mice, SuFEx‐modified flavonoids improved glycemic control, preserved pancreatic integrity, and remodeled gut microbiota composition, restoring microbial diversity and metabolic function. This work validates SuFEx‐enabled covalent reprogramming as a powerful strategy to transform dietary natural products into precision metabolic medicines, offering a versatile platform for developing selective, microbiota‐compatible metabolic therapeutics.