Archives of oral biology · 2021
Asperuloside ameliorates lipopolysaccharide-induced primary human periodontal ligament cell injury by decreasing TLR4 expression and NF-κB activation.
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Fan Xiaodan, Zhou Chun, Huang Cheng, Zhang Junye
Аннотация
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.
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.