Stroke is one of the leading causes of death and disability worldwide. However, information on stroke-related tongue coating microbiome (TCM) is limited, and whether TCM modulation could benefit for stroke prevention and rehabilitation is unknown. Here, TCM from stroke patients (SP) was characterized using molecular techniques. The occurrence of stroke resulted in TCM dysbiosis with signif icantly reduced species richness and diversity. The abundance of Prevotella, Leptotrichia, Actinomyces, Alloprevotella, Haemophilus, and TM7_[G-1]were greatly reduced, but common infection Streptococcus and Pseudomonas were remarkably increased. Furthermore, an antioxidative probiotic Lactiplantibacillus plantarum AR113 was used for TCM intervention in stroke rats with cerebral ischemia/reperfusion (I/R). AR113 partly restored I/R induced change of TCM and gut microbiota with significantly improved neurological deficit, relieved histopathologic change, increased activities of antioxidant enzymes, and decreased contents of oxidative stress biomarkers. Moreover, the gene expression of antioxidant-related proteins and apoptosis-related factors heme oxygenase-1 (HO-1), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), nuclear factor erythroid 2-related factor 2 (Nrf2), NAD(P)H:quinone oxidoreductase-1 (NQO-1), and Bcl-2 was significantly increased, but cytochrome C, cleaved caspase-3, and Bax were markedly decreased in the brain by AR113 treatment. The results suggested that AR113 could ameliorate cerebral I/R injury through antioxidation and anti-apoptosis pathways, and AR113 intervention of TCM may have the application potential for stroke prevention and control.

Probiotics could effectively eliminate excess reactive oxygen species (ROS) generated during aging or lipid metabolism disorders, but their mechanism is unclear. The major purpose of this study was to investigate the mechanism of Lactiplantibacillus plantarun AR113 alleviating oxidative stress injury in the D-galactose induced aging mice. The result showed that pretreatment with L. plantarun AR113 significantly relieving H₂O₂ induced cytotoxicity in HepG2 cells by maintain cell membrane integrity and increasing antioxidant enzyme activities. In D-galactose induced aging mice, L. plantarun AR113 could significantly attenuate liver damage and inf lammatory infiltration by promoting endogenous glutathione (GSH) synthesis and activating the Nrf2/Keap1 signaling pathway in mice, and increasing the expression of regulated phase Ⅱ detoxification enzymes and antioxidant enzymes. Further analysis shown that gavage of L. plantarun AR113 could significantly reduce the expression of G protein-coupled receptor 78 (GPR78) and C/EBP homologous protein(CHOP) proteins, and promote the restoration of endoplasmic reticulum (ER) homeostasis, thereby activating cell anti-apoptotic pathways. These results were also confirmed in H₂O₂-treated HepG2 experiments. It indicated that L. plantarun AR113 could inhibit D-galactose-induced liver injury through dual inhibition of ER stress and oxidative stress. L. plantarun AR113 have good application potential in anti-aging and alleviating metabolic disorders.