Mitochondrial Calcium Nanoregulators Reverse The Macrophage Phenotype In Periodontitis

Design and apply nanomaterials to inhibit tissue inflammation response and promote tissue regeneration based on mitochondrial calcium overload in macrophages of periodontitis. Calcium overload of macrophage mitochondria was detected by the fluorescent probe. Fluorescence colocalization was used to evaluate METP nanoparticle uptake by macrophages. Mitochondrial calcium levels, endoplasmic reticulum and cytoplasmic calcium levels were measured in vitro after LPS stimulation. Proinflammatory phenotypes of macrophages were detected by surface markers, cytokine secretion, and intracellular inflammatory gene transcription and protein expression. The effect of METP nanoparticles on macrophage metabolism was investigated by Seahorse cell energy metabolism experiment. METP nanoparticles were injected into periodontal area to verify the inhibitory effect on inflammation. This study demonstrated that METP nanoparticles reversed calcium overload in mitochondria and proinflammatory phenotype of macrophages by inhibiting mitochondrial aspart-arginine succinic acid shingling and ROS production. In this study, we synthesized MSN-EGTA-TPP-PEG (METP) nanoparticles, which could specifically target mitochondria and block excessive calcium ion inflow, and achieved inhibition of inflammation in mice periodontitis and promoted the regeneration of alveolar bone tissue.