We aimed to investigate whether curcumin can employ the phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B (Akt) signaling pathway to relieve inflammation in human dental pulp cells (hDPCs) mediated by lipopolysaccharide (LPS). The surface markers of hDPCs were detected by immunofluorescence assay. The toxicity of curcumin and LPS on hDPCs was determined using the methyl thiazolyl tetrazolium assay. The cells were treated with LPS and randomized to Control group (cultured with DMEM), LPS group (culture with 1 μg/ml LPS-containing medium), Cru-L group (incubation with medium containing 1 μg/ml LPS and 5 μmol/l curcumin), Cru-M group (incubation with medium containing 1 μg/ml LPS and 10 μmol/l curcumin), Cru-H group (incubation with medium containing 1 μg/ml LPS and 30 μmol/l curcumin), and Cru-H+SC79 group (incubation with medium containing 1 μg/ml LPS, 30 μmol/l curcumin and SC79 10 μmol/l). The cell counting kit-8 assay for hDPC survival rate and flow cytometry for hDPC apoptosis rate were implemented. The Cru-L group, Cru-M group and Cru-H group, in comparison to the LPS group, had a significantly raised cell survival rate, along with significant decreases in the phosphorylated protein kinase B (p-Akt)/Akt ratio, apoptosis rate, IL-6, IL-1β and TNF-α levels, and p-PI3K/PI3K ratio (P<0.05). In comparison with the Cru-H group, the Cru-H+SC79 group had a significantly decreased cell survival rate, and significantly increased p-PI3K/PI3K ratio, apoptosis rate, p-Akt/Akt ratio, and IL-6, IL-1β and TNF-α levels (P<0.05). Curcumin can suppress the PI3K/Akt signaling pathway to mitigate LPS-induced inflammation of hDPCs, thus relieving the inflammatory injury of dental pulp tissues.
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