Metabolic-associated fatty liver disease (MAFLD), a global health burden with limited therapeutic options beyond lifestyle changes, urgently needs novel strategies. We engineered exosome-like nanovesicles (HNVs) from dried honeysuckle (Lonicera japonica), exhibiting significantly more uniform size distribution than conventional herbal extracts and characteristic nanovesicle morphology. Orally delivered HNVs, enriched with bioactive metabolites, dramatically inhibited increased fat vacuoles, lipid droplet deposition, and collagen fibrosis in the livers of mice with MAFLD induced by high-fat diet (HFD). Mechanistically, HNVs orchestrate a dual gut-liver intervention: (1) restoring gut barrier integrity, slashing serum LPS by 1.58-fold and quelling hepatic inflammation; (2) remodeling gut microbiota to suppress bile salt hydrolase (BSH), elevating taurochenodeoxycholic acid (TCDCA) 2.07-fold. This microbial shift reprograms enterohepatic signaling by inhibiting the FXR-FGF15-FGFR4 axis, thereby boosting hepatic cholesterol catabolism via bile acid synthases. Critically, efficacy is strictly microbiota-dependent: abolished by antibiotics and fully transferable via fecal microbiota transplantation (FMT) from HNV-treated donors. Presenting the first natural nanovesicle platform that concurrently targets gut barrier repair and metabolic reprogramming, HNVs establish a pioneering, multi-targeted therapeutic paradigm for MAFLD, directly linking gut microbial ecology to hepatic pathophysiology with high translational potential.

Uncontrollable bleeding and bacterial infections are the major reasons for the high mortality of post-traumatic. In this study, a composite hemostatic chitosan sponge CaO₂@SiO₂/CS was prepared by combining a novel core–shell inorganic nano hemostatic CaO₂@SiO₂ nanoparticles with carboxylated chitosan, which presents a multi-layered structure with a rough and hydrophilic surface for rapid absorption of blood. When the CaO₂@SiO₂ nanoparticles in the CaO₂@SiO₂/CS come into contact with blood, the silanol group on its surface and the released H₂O₂ and Ca²⁺ can recruit and activate platelets, while generating fibrin clots and activating the endo-exogenous coagulation cascade reaction to achieve rapid clotting. The H₂O₂ released from CaO₂@SiO₂ shows the antimicrobial capacity and stimulates the production of tissue factors by endothelial cells. Meanwhile, the silica coating reduces the cytotoxicity of bare CaO₂, thus reducing the risk of secondary bleeding at the site of vascular injury. CaO₂@SiO₂/CS (48 s) showed a 1.83- and 2.52-fold reduction in hemostasis time compared to commercial gelfoam and CS in a femoral artery hemorrhage model. This study illustrates the hemostatic mechanism of CaO₂@SiO₂ and provides a reference for the development of clinical biomedical inorganic hemostatic materials.