Abstract:

Objective This study aimed to explore the role and mechanism of silibinin in renal injury induced by periodontitis. Methods Twenty-four male C57BL/6J mice were randomly divided into three groups: normal control (Control), periodontitis (P), and periodontitis+silibinbin intervention (P+SB). Ligation with 7-0 silk thread around the maxillary second molar’s neck was performed to generate a periodontitis animal model. Hematoxylin-eosin (HE), Masson staining, and micro-CT techniques were used to verify the successful construction of the periodontitis model. Renal injury degree was evaluated by renal histological exa-mination (HE, periodic acid-schiff, and Masson staining), ultrastructure observation under a transmission electron microscope, and blood biochemical index detection. The balance of oxidation and antioxidation in kidney tissue was observed by detecting the index of oxidative stress and MitoSOX Red fluorescence staining. The mRNA expression of mammalian target of rapamycin (mTOR) was detected by quantitative reverse transcription polymerase chain, and the localization and expression of mTOR in mouse kidney was further clarified using immunohistochemical staining. Results Compared with that in the Control group, gingival destruction and inflammation around the second molar were more evident in the P group. The alveolar bone was absorbed remarkably, as characterized by a decrease in bone volume fraction (BV/TV) and trabecular thickness and the widening of trabecular spacing. Renal tissue showed signs of renal injury, such as widening of Bowman space, exfoliation of renal tubular epithelial cells, morphological destruction of foot process, swel-ling of mitochondria, and disappearance of mitochondrial crest, accompanied with a significant increase in malondialdehyde (MDA) level, a decrease in glutathione (GSH) and superoxide dismutase (SOD) activities, and the activation of mTOR signal pathway. In the P+SB group, the destruction of gingiva and alveolar bone was significantly reduced, kidney injury was effectively alleviated, the MDA level decreased, SOD and GSH activities were recovered, and the mTOR signal pathway was significantly inhibited. Conclusion Silibinin can effectively alleviate the oxidative stress injury of kidney and alleviate the renal injury caused by periodontitis by regulating the mTOR signal pathway.

Key words: periodontitis, oxidative stress, kidney injury, silibinin, mammalian target of rapamycin signal pathway