Abstract

To investigate the mechanism of linagliptin on stromal cell-derived factor 1 and vascular endothelial growth factor protein after molar pulp revascularization in rats. 45 specific-pathogen free male Sprague-Dawley rats were divided into 5 groups based on the average body weight, with 9 rats in each group. The control group did not establish the rat model of molar pulp revascularization, and model group, low-linagliptin group, mediumlinagliptin group, and high-linagliptin group all established the rat model of molar pulp revascularization. On d 1 after modeling, rats in low-linagliptin group, medium-linagliptin group, and high-linagliptin group were gavaged with 1, 2, and 3 mg/ml linagliptin, respectively. Rats in control group and model group were gavaged with 0.9 % normal saline at equal volume, once a day for 28 d. After the last gavage, the rats were detected for the body weight and fasting blood glucose, and superoxide dismutase and serum oxidative stress indicators malondialdehyde were detected by kit; hematoxylin and eosin staining was employed to detect the pathological morphology of dental pulp tissue, immunohistochemistry and immunoblot were applied to detect the positive expression of vascular endothelial growth factor and stromal cell-derived factor 1 and the protein content. No significant differences were found in fasting blood glucose and body weight between the groups (p>0.05). In control group, loose connective tissue was found in the root canal of rats, and a large number of long spindle forming fibrocytes were distributed; in model group, a large number of inflammatory cells are found under the dental pulp, with the majority of neutrophils; in comparison with model group, inflammatory cells in pulp tissue of low-linagliptin group, medium-linagliptin group and high-linagliptin group gradually decreased, and scattered restorative dentin could be found in the pulp, and there was no inflammatory expression in the middle and lower tissues of the pulp. Dipeptidyl peptidase 4 inhibitor linagliptin has no effect on rats’ body weight and blood glucose after revascularization, but it can improve the level of oxidative stress and accelerate revascularization and perhaps its mechanism links to the up-regulation of vascular endothelial growth factor and stromal cell-derived factor 1 expression.