This study found that agarononaose (A9) exhibits the most significant anti-senescence effect on HL-1 cardiomyocytes among agarose-derived oligosaccharides. Meanwhile, we found that this feature appears to be associated with the mechanism of nutritional intervention dysregulation. Further investigation revealed that A9 improved a series of mitochondrial mechanisms, including oxidative phosphorylation (OXPHOS), mitochondrial membrane potential, oxidative stress, the mitochondrial unfolded protein response (UPR mt ), mitochondrial biogenesis, and mitochondrial dynamics. Importantly, through mitochondrial transplantation experiments and OXPHOS inhibition, it was demonstrated that the enhancement of OXPHOS is a primary mechanism through which A9 ameliorates cellular senescence. Moreover, this bioactivity could be transferred to recipient cells via mitochondrial transplantation. This study identifies a natural marine oligosaccharide as a potential functional food and pharmaceutical agent for ameliorating cardiac cell senescence, and elucidates its key mechanisms. Furthermore, we propose a novel research approach based on mitochondrial transplantation for investigating drug interventions targeting mitochondrial function. • A9 exhibits the strongest activity in delaying the senescence of cardiomyocytes. • A9 localizes to mitochondria after entering cells. • A9 extensively improved mitochondrial function. • A9 may exert its biological effects by enhancing oxidative phosphorylation.

Tannic acid (TA) demonstrates therapeutic potential for gastroenteritis, but its efficacy against ulcerative colitis (UC) remains unclear. This study evaluated the protective effects of TA against dextran sulfate sodium (DSS)-induced murine colitis. Mice were administered TA (20, 40, or 80 mg/kg) or sulfasalazine (SASP). TA treatment significantly ameliorated colitis severity, as demonstrated by improved body weight recovery, reduced disease activity index (DAI), and attenuated colon shortening. Mechanistically, TA suppressed oxidative stress and inhibited the NF-κB signaling pathway, thereby reducing inflammatory responses. Additionally, TA enhanced intestinal barrier function through increased expression of key tight junction proteins. Furthermore, TA administration dose-dependently remodeled the gut microbiota, with low and medium doses (20 and 40 mg/kg) exhibiting efficacy comparable or superior to SASP. These findings indicate that TA ameliorates DSS-induced colitis through synergistic antioxidant, anti-inflammatory, and microbiota–modulatory actions, highlighting its potential as a natural therapeutic or adjunctive agent for UC. • Tannic acid ameliorates DSS-induced colitis via improved body weight, colon length and DAI. • Tannic acid inhibits oxidative stress and inflammation via NF-κB pathway inhibition. • Tannic acid reinforces the intestinal barrier via mucus and tight junction upregulation. • Tannic acid beneficially remodels the gut microbiota, with lower doses showing optimal efficacy.