Budesonide and Poractant Alfa prevent bronchopulmonary dysplasia via triggering SIRT1 signaling pathway.

OBJECTIVE: This study aimed to evaluate effect of budesonide combining Poractant Alfa on preventing bronchopulmonary dysplasia (BPD). PATIENTS AND METHODS: A total of 120 preterm infants were involved. pH value, partial pressure of oxygen (PO2), and blood gas analysis were evaluated. Peripheral blood was collected and mononuclear cells were isolated. Reactive oxygen species (ROS) in peripheral blood mononuclear cells (PBMCs) were detected with laser confocal. Sirtuin 1 (SIRT1) in PBMCs was detected using immunofluorescence. SIRT1 and small ubiquitin-like modifier (SUMO)-specific protease 1 (SENP1) were detected with Western blot. RESULTS: Compared with group B, pH value and PO2 were improved significantly in group C and D (p<0.01). Compared with group B, oxygen inhalation duration, rate of having a respirator assisted ventilation, and using pulmonary surfactant (PS) again, and BPD incidence were significantly decreased in other groups (p<0.05). BPD incidence in group D was less than group C (χ2=4.00, p<0.05). Compared with control group, ROS level of neonatal respiratory distress syndrome (NRDS) group was significantly increased, SENP1 was increased, and SIRT1 was decreased in SIRT1 group. Compared with NRDS, when budesonide combined with Poractant Alfa, ROS decreased, SENP1 decreased, SIRT1 nuclear pulp shuttling rate reduced, nuclear SIRT1 increased (p<0.01). Compared with control, ROS level of NRDS group was significantly increased, SENP1 increased, and SIRT1 in nucleus decreased (p<0.05). Compared with NRDS group, when treated with budesonide and Poractant Alfa, ROS levels decreased, SENP1 decreased, nuclear SIRT1 increased (p<0.01). CONCLUSIONS: Budesonide combining Poractant Alfa can prevent BPD in preterm infants by activating the SIRT1 signaling pathway.

Effects of insulin-like growth factor I on alveolar bone remodeling in diabetic rats.

BACKGROUND AND OBJECTIVE: Diabetes is a chronic hyperglycemic disorder and results in a tendency to develop osteoporosis. Furthermore, the delayed healing of tooth-extraction wounds, the activation of alveolar resorption and the suppressed formation of bone around implants are difficult for dentists to resolve. In diabetes, insulin-like growth factor I (IGF-I) appears to enhance the differentiation of osteoblasts and to activate the mineralization of bone. Hence, the aim of this study was to investigate the effects of insulin-like growth factor I on the remodeling of alveolar bone in diabetic rats. MATERIAL AND METHODS: Diabetes was induced in 40 male Sprague-Dawley rats by intravenous administration of alloxan. The teeth of the rats were extracted to investigate remodeling of alveolar bone. Insulin-like growth factor I was administered, via intraperitoneal injection, to diabetic rats following tooth extraction. The remodeling of alveolar bone was determined using radiographic data, histological analyses and tetracycline fluorescence labeling. RESULTS: Compared with the control group, diabetes decreased alveolar bone formation. The height of alveolar bone and the bone-formation rate was significantly lower in the untreated diabetic group than in the control group or in the treated rats. Treatment with insulin-like growth factor I not only regulated abnormal blood glucose levels but also increased the height of the alveolar bone and increased the bone-formation rate relative to the results in diabetic animals. Furthermore, the expression of glucose transporter-1, the main transporter of glucose, was changed by hyperglycemia. CONCLUSION: The results suggest that insulin-like growth factor I treatment increases the volume of newly formed bone following tooth extraction and normalizes the expression of glucose transporter-1 in diabetic rats, which may play an important role in bone formation and mineralization.