¹Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210018, Jiangsu Province, China
²Guiyang Stomatological Hospital, Guiyang 550000, Guizhou Province, CHINA DOI : 10.9775/kvfd.2023.29397 Pulpitis refers to the inflammation of dental pulp tissues caused by infection with dental caries. We aimed to evaluate the effects of micro ribonucleic acid (miR)-155 on inflammatory response and autophagy upon pulpitis via the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) signal. Forty rats were randomly assigned to negative control (NC), pulpitis model (PM), anti-miR-155, and anti-miR-155+diethyldithiocarbamate (DDC) groups (n=10). Primary human dental pulp cells were divided into NC, lipopolysaccharide (LPS), anti-miR-155, and DDC groups. Compared with the PM group, the IL-1β, TNF-α, and MDA levels and pulp necrosis rate decreased, while the SOD activity was enhanced in the anti-miR-155 group (P<0.05). Compared to the NC group, the positive expressions of LC3B and Beclin1 and the protein expressions of NLRP3 and Caspase-1 significantly rose in the PM group (P<0.05). Compared with the PM group, the protein expressions of NLRP3 and Caspase-1 significantly decreased, and the positive expressions of LC3B and Beclin1 increased in the anti-miR-155 group (P<0.05). Compared with the anti-miR-155 group, the DDC group had significantly enhanced activity of dental pulp cells, up-regulated mRNA levels of IL-1β, TNF-α, NLRP3, and Caspase-1, and decreased mRNA levels of LC3B and Beclin1 (P<0.05). Suppressing miR-155 expression can relieve inflammatory response and promote autophagy. Anahtar Kelimeler : Autophagy, Inflammatory response, MicroRNAs, Pulpitis