Carnosic Acid In Diabetic Periodontitis: Mechanisms And Effects

To investigate the potential of carnosic acid as a novel therapeutic agent for diabetic periodontitis by regulating macrophage oxidative stress and autophagy. The study used in vitro and in vivo methods to explore carnosic acid's effects on macrophage oxidative stress and autophagy in diabetic periodontitis (DP). In vitro, RAW264.7 macrophages were cultured under high-glucose conditions with lipopolysaccharide stimulation to mimic DP inflammation. The impact of carnosic acid on oxidative stress markers, autophagy proteins, and inflammatory cytokines was assessed using Western blot and RT-PCR. In vivo, a rat DP model was induced with high-fat diet, streptozotocin, and ligature. Clinical indices, Micro-CT, and histology were used to evaluate carnosic acid's therapeutic effects. The goal was to determine carnosic acid's potential as a DP treatment. In vitro, carnosic acid significantly reduced ROS levels. It also promoted autophagy by increasing the LC3-II/I ratio and decreasing p62 expression, while inhibiting inflammatory cytokines TNF-α, IL-1β, and IL-6. In vivo, carnosic acid treatment in diabetic periodontitis rats resulted in reduced clinical indices of periodontitis, decreased alveolar bone loss, and improved histological outcomes, demonstrating its therapeutic potential. Carnosic acid regulates macrophage oxidative stress and autophagy in diabetic periodontitis, suggesting its potential as a therapeutic agent for DP.