Asperuloside ameliorates lipopolysaccharide-induced primary human periodontal ligament cell injury by decreasing TLR4 expression and NF-κB activation. (September 2021)

• Record Type: Journal Article
• Authors: Fan, Xiaodan; Zhou, Chun; Huang, Cheng; Zhang, Junye
• Is Part Of: Archives of oral biology. Volume 129(2021)
• Publication Date: 2021-09
• Subjects: LPS lipopolysaccharide -- CP chronic periodontitis -- ASP asperuloside -- TLR4 Toll-like receptor 4 -- PDLCs primary human periodontal ligament cells -- IL-1β interleukin-1β -- IL-6 interleukin 6 -- IL-8 interleukin 8 -- TNF- tumor necrosis factor alpha -- BOP bleeding on probing -- REC gingival recession -- CAL clinical attachment level -- PD probing depth -- MAPK mitogen-activated protein kinase -- TRIM tripartite motif-containing -- NF-κB nuclear transcription factor κB; Asperuloside -- Lipopolysaccharide -- Chronic periodontitis -- TLR 4 -- NF-κB; Mouth -- Periodicals; Mouth -- Diseases -- Periodicals; Dentistry -- Periodicals; Electronic journals; 617.6005
• DOI: 10.1016/j.archoralbio.2021.105199
• Languages: English
• ISSNs: 0003-9969

Abstract

Highlights: ASP alleviated LPS-induced CP progression both in gingival tissue and in PDLCs. TLR4 mediated LPS-induced CP progression through the TLR4/NF-κB signaling pathway. Overexpression of TLR4 blocked the protective effect of ASP in LPS-induced CP. Abstract: 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 LPS-induced 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)-1β, IL-6, IL-8 and tumor necrosis factor alpha (TNF-α). 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-κB activation, while this protective effect of ASP was reversed by TLR4 overexpression.