Antibiotic resistance has emerged as a critical global public health challenge. In this study, we employed metagenomic sequencing to analyze fecal samples from giant pandas (Ailuropoda melanoleuca) across three distinct stages—semi-wild, released, and wild populations—to investigate shifts in antibiotic resistance genes (ARGs) and virulence factors (VFs) during the reintroduction process. Our findings revealed significant variations in the composition of ARG and VF across different stages, with released and wild giant pandas exhibiting similar ARG and VF profiles. Further analyses identified that the increased abundance of ARGs and VFs in both released and wild individuals compared to semi-wild individuals was mainly from Pseudomonas. We hypothesized that the same geographic environment in which ARGs and VFs are transmitted between a host and the environment via mobile genetic elements (MGEs) may be responsible for the similar structure of ARGs and VFs in released and wild giant pandas. Additionally, diet may modulate the gut microbial community, thereby influencing the distributions of ARG and VF. This study elucidated the impact of geographic and dietary factors on ARGs and VFs dynamics in giant pandas, offering valuable insights for mitigating antibiotic resistance and virulence gene dissemination.
Background: Renal aging represents a pivotal contributor to the pathogenesis and progression of age-related kidney disorders. D-Pinitol (DP), a bioactive cyclitol naturally present in food plants, exhibits multiple beneficial biological activities. Nevertheless, its role in counteracting renal aging remains unclear. Methods: This study employed both in vitro (HK-2 cells) and in vivo (C57BL/6J mice) models of D-galactose (DG)-induced renal aging. A panel of experimental approaches was applied to characterize the protective effects and molecular mechanisms of DP against renal aging, including Western blot, qPCR, ELISA, transcriptomic profiling, transmission electron microscopy, surface plasmon resonance (SPR), immunohistochemistry, and immunofluorescence staining. Results: DP significantly attenuated DG-induced renal aging-like changes in vitro and in vivo by preserving mitochondrial function and alleviating inflammatory responses. Transcriptomic analysis suggested SARM1 as a potential key target responsible for the beneficial effects of DP. In DG-induced aging models, SARM1 was remarkably upregulated in a tubule-specific pattern and acted as a critical mediator of mitochondrial dysfunction. Damaged mitochondria released mtDNA, which further activated the cGAS–STING innate immune signaling pathway, consequently promoting the senescence-associated secretory phenotype (SASP) and renal inflammation. Mechanistically, molecular docking and related assays suggested that DP may stabilize the auto-inhibitory conformation of SARM1, thereby potentially preventing its activation. Conclusions: DP attenuates DG-induced renal aging-like changes via suppressing the SARM1–cGAS–STING axis, thereby restoring mitochondrial homeostasis and mitigating inflammation. Given the lack of effective interventions targeting renal aging, these findings suggest SARM1 as a novel potential therapeutic target for renal aging and highlight DP as a promising food-derived anti-aging ingredient for renal protection.