Asperuloside ameliorates lipopolysaccharide-induced primary human periodontal ligament cell injury by decreasing TLR4 expression and NF-KB activation

Objective: The mechanism underlying lipopolysaccharide (LPS)-induced primary human periodontal ligament (PDLC) cell injury is unclear. In this study, we focused on the therapeutic function of asperuloside (ASP) on LPSinduced cell injury. Design: The study enrolled 41 participants, including 18 healthy controls and 23 CP patients. Western blotting was used to measure the expression of Toll-like receptor 4 (TLR4), phosphorylated p65 (p-p65) and cyclin D1. Enzyme-linked immunosorbent assays (ELISAs) were utilized to evaluate the protein levels of proinflammatory factors interleukin (IL)-113, IL-6, IL-8 and tumor necrosis factor alpha (TNF-a). MTT assays and 5-ethynyl-2 ' deoxyuridine (EdU) staining were performed to investigate cell proliferation. Immunohistochemistry was used to detect TLR4 and p65 expression in gingival tissues. Results and conclusions: Asperuloside ameliorates lipopolysaccharide-induced PDLC cell injury by decreasing TLR4 expression and NF-KB activation, while this protective effect of ASP was reversed by TLR4 overexpression.