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Jun Wang, Yi Du, Junhong Deng, Xin Wang, Fei Long, Jianmin He
(Stomatological Center, Gansu Provincial Hospital, Lanzhou, Gansu, China (mainland))
Med Sci Monit 2019; 25:10008-10015
Toothache often occurs with pulpitis. Lipopolysaccharide (LPS) is produced by gram-negative bacteria, and its accumulation is related to clinical symptoms of pain. MicroRNAs (miRNAs) display anti-inﬂammatory potential due to their direct regulation of cellular protein expression, which can promote inﬂammatory changes in dental pulp tissues. However, the mechanism of LPS-induced pulpitis is still unclear.
MATERIAL AND METHODS: In this study, dental pulp stem cells (DPSCs) were separated and cultured from rat dental pulp tissues; then, LPS was administered to induce inflammation and activate the TLR4 pathway.
RESULTS: It was found that miR-506 was upregulated following LPS treatment in DPSCs. The inhibition of miR-506 in LPS-treated DPSCs led to attenuated inflammation and deactivation of the TLR4 pathway. Furthermore, the bioinformatic analysis and dual-luciferase reporter gene assay indicated that miR-506 could target the 3’-UTR of sirtuin 1 (SIRT1). Additionally, SIRT1 decreased in LPS-treated DPSCs, and miR-506 transfection resulted in SIRT1 upregulation. SIRT1 overexpression showed a similar inhibitory effect as that of miR-506 downregulation on inflammation and TLR4 activation in DPSCs.
CONCLUSIONS: In brief, miR-506 can protect dental pulp in LPS-induced inflammation by inhibiting the SIRT1-mediated TLR4 pathway.