The Protective Effects of S14G-humanin (HNG) Against Lipopolysaccharide (LPS)- Induced Inflammatory Response in Human Dental Pulp Cells (hDPCs) Mediated by the TLR4/MyD88/NF-κB Pathway

Overview

Journal Bioengineered

Date 2021 Oct 4

PMID 34605740

Citations 5

Authors

Ping Zhang

Zhiqiang Cui

Shuai Li

Affiliations

Soon will be listed here.

Abstract

Pulpitis is reported in large populations of patients and significantly impacts their normal life quality. It is reported that the lipopolysaccharide (LPS) in Gram-negative bacteria induces severe inflammation in dental pulp tissues. S14G-humanin is a derivative of humanin and has been recently confirmed to possess promising anti-inflammatory properties. The current study aims to explore the possibility of treating pulpitis with S14G-humanin. LPS-stimulated dental pulp cells (DPCs) were utilized to simulate an inflammatory state in the progression of pulpitis. We found the elevated expressions and production of interleukin- 6 (IL-6), tumor necrosis factor-α (TNF-α), macrophage chemoattractant protein-1 (MCP-1), matrix metalloproteinase-2 (MMP-2), and matrix metalloproteinase-9 (MMP-9), upregulated Pentraxin 3 (PTX3) and activated oxidative stress in LPS-treated DPCs were all reversed by treatment with 50 and 100 μM S14G-humanin. In addition, the LPS-induced elevated expression levels of toll-like receptor 4 (TLR4) and myeloid differentiation primary response 88 (Myd88), and activation of the IκBα/NF-κB signaling pathway in hDPCs were significantly repressed by treatment with S14G-humanin. Conclusively, we found that S14G-humanin protected LPS-treated hDPCs by inhibiting the TLR4/MyD88/NF-κB signaling pathway.

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