Ginsenoside Rb1 alleviates lipopolysaccharide‐induced inflammation in human dental pulp cells via the PI3K/Akt, NF‐κB, and MAPK signalling pathways

Abstract

AbstractAimAmong numerous constituents of Panax ginseng, a constituent named Ginsenoside Rb1 (G‐Rb1) has been studied to diminish inflammation associated with diseases. This study investigated the anti‐inflammatory properties of G‐Rb1 on human dental pulp cells (hDPCs) exposed to lipopolysaccharide (LPS) and aimed to determine the underlying molecular mechanisms.MethodologyThe KEGG pathway analysis was performed after RNA sequencing in G‐Rb1‐ and LPS‐treated hDPCs. Reverse‐transcription polymerase chain reaction (RT–PCR) and western blot analysis were used for the assessment of cell adhesion molecules and inflammatory cytokines. Statistical analysis was performed with one‐way ANOVA and the Student–Newman–Keuls test.ResultsG‐Rb1 did not exhibit any cytotoxicity within the range of concentrations tested. However, it affected the levels of TNF‐α, IL‐6 and IL‐8, as these showed reduced levels with exposure to LPS. Additionally, less mRNA and protein expressions of vascular cell adhesion molecule‐1 (VCAM‐1) and intercellular adhesion molecule‐1 (ICAM‐1) were shown. With the presence of G‐Rb1, decreased levels of PI3K/Akt, phosphorylated IκBα and p65 were also observed. Furthermore, phosphorylated ERK and JNK by LPS were diminished within 15, 30 and 60 min of G‐Rb1 exposure; however, the expression of non‐phosphorylated ERK and JNK remained unchanged.ConclusionsG‐Rb1 suppressed the LPS‐induced increase of cell adhesion molecules and inflammatory cytokines, while also inhibiting PI3K/Akt, phosphorylation of NF–κB transcription factors, ERK and JNK of MAPK signalling in hDPCs.