A novel fluorescent probe for detecting hydrogen sulfide in osteoblasts during lipopolysaccharide-mediated inflammation under periodontitis

Xiaoya Lu,Hanchuang Zhu,Yue Wu,Dongsheng Zhang,Yi Chen,Shengyun Huang,Baocun Zhu

doi:10.1038/s41598-021-99761-4

Xiaoya Lu, Hanchuang Zhu + Show 5 more

Open Access

https://doi.org/10.1038/s41598-021-99761-4

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Abstract

Periodontitis, one of the most common chronic inflammatory diseases, affects the quality of life. Osteogenesis plays an important role in the disease. There is a connection between hydrogen sulfide (H2S) and periodontitis, but according to the study has been published, the precise role of H2S in inflammation remains in doubt. The main reason for the lack of research is that H2S is an endogenous gasotransmitter, difficult to discern through testing. So, we synthesized a novel fluorescence probe which can detect H2S in vitro. By using the novel H2S fluorescence probe, we found that H2S changes in osteoblasts mainly by cystathionine-γ-lyase, and H2S increases under LPS stimulation. H2S could be a potential marker for diagnosis of inflammatory diseases of bone, and might help deepen studies of the changes of H2S level and promote the progression on the researches about pathogenesis of periodontitis.

Highlights

Periodontitis as one of the most common chronic inflammatory diseases, afflicting man
H 2S is produced by the sulfur-containing materials cysteine, homocysteine or 3-mercaptopyruvate. H2S is transformed by cystathionine-β-synthase (CBS), cystathionine-γ-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3-MST)[6]
For exogenous H 2S, it can promote LPS-induced apoptosis of osteoblast cells, which might represent a new direction in the treatment of o steomyelitis[8]

Summary

Introduction

Periodontitis as one of the most common chronic inflammatory diseases, afflicting man. The balance of osteoclasts and osteoblasts is tightly related to avoid the loss of bone. Lipopolysaccharide (LPS), a major toxic factor of gram-negative bacteria, plays a main role in periodontitis. It can cause periodontitis by modulating the activity of the host d efenses[1], inducing a hypoxic p hase[2] etc., and it eventually stimulates bone r esorption[3]. LPS may lead to inflammatory response in osteoblasts and osteoblasts, which may results in a disorder in the balance of osteoclasts and osteoblasts even cell death, leading to accelerating bone loss[4]. There is a connection between H2S and periodontitis, but until now, the precise role of H 2S in inflammation remains unknown

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