IADR Abstract Archives
Silibinin Attenuated Diabetic Periodontitis Through Preservation of Mitochondrial Function
Objectives: Diabetic periodontitis (DP), a major complication of diabetes, demonstrates increased incidence and severity of periodontal destruction compared to periodontitis. Mitochondrial oxidative stress and dysfunction have a crucial role in the pathogenesis of DP. Silibinin exerts strong antioxidant and mitochondria-protective properties. Our aim was to investigate the effect of silibinin on DP and the underlying molecular basis thereof.
Methods: Wistar rats were randomly assigned into groups: control, diabetes, diabetic periodontitis, and diabetic periodontitis with silibinin treatment. All rats were provided 0.5% sodium carboxymethyl cellulose or silibinin for four weeks after the induction of diabetes. Two weeks after induction of diabetes, periodontitis was induced by silk ligation for 2 weeks and thereafter evaluated by assessing alveolar bone loss and apoptosis of periodontal cells. Mitochondrial oxidative stress was detected by MitoSOX staining. Mitochondrial function was determined by measuring ATP production, and by assessing mitochondrial DNA copy number, expression of electron transport chain complexes, and biogenesis with real-time PCR.
Results: Pathological examination revealed that silibinin mitigated alveolar bone loss and periodontal cell apoptosis involved in DP. Additionally, silibinin improved mitochondrial function, as evidenced by decreased generation of reactive oxygen species in mitochondria, enhanced adenosine triphosphate production, augmented mitochondrial DNA copy number, increased expression of electron transport chain complex I, and enhanced mitochondrial biogenesis. Furthermore, the expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) was downregulated and closely related with mitochondrial dysfunction in rats with DP and also in the apoptosis model of periodontal ligament cells. More importantly, the decreased expression of PGC-1α could be reversed by silibinin.
Conclusions: Taken together, DP could be attenuated by silibinin through the preservation of PGC-1α dependent mitochondrial function, which lays a strong foundation for the clinical application of silibinin to treat DP.
Methods: Wistar rats were randomly assigned into groups: control, diabetes, diabetic periodontitis, and diabetic periodontitis with silibinin treatment. All rats were provided 0.5% sodium carboxymethyl cellulose or silibinin for four weeks after the induction of diabetes. Two weeks after induction of diabetes, periodontitis was induced by silk ligation for 2 weeks and thereafter evaluated by assessing alveolar bone loss and apoptosis of periodontal cells. Mitochondrial oxidative stress was detected by MitoSOX staining. Mitochondrial function was determined by measuring ATP production, and by assessing mitochondrial DNA copy number, expression of electron transport chain complexes, and biogenesis with real-time PCR.
Results: Pathological examination revealed that silibinin mitigated alveolar bone loss and periodontal cell apoptosis involved in DP. Additionally, silibinin improved mitochondrial function, as evidenced by decreased generation of reactive oxygen species in mitochondria, enhanced adenosine triphosphate production, augmented mitochondrial DNA copy number, increased expression of electron transport chain complex I, and enhanced mitochondrial biogenesis. Furthermore, the expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) was downregulated and closely related with mitochondrial dysfunction in rats with DP and also in the apoptosis model of periodontal ligament cells. More importantly, the decreased expression of PGC-1α could be reversed by silibinin.
Conclusions: Taken together, DP could be attenuated by silibinin through the preservation of PGC-1α dependent mitochondrial function, which lays a strong foundation for the clinical application of silibinin to treat DP.