SPRC Suppresses Experimental Periodontitis by Modulating Th17/Treg Imbalance

Area of Science:

• Biochemistry
• Immunology
• Periodontology

Background:

• Periodontitis is a chronic inflammatory disease causing alveolar bone destruction.
• Hydrogen sulfide (H2S) plays a role in inflammatory conditions.
• The balance between Th17 and Treg cells is crucial in periodontitis pathogenesis.

Purpose of the Study:

• To investigate the protective effects of S-propargyl-cysteine (SPRC) on periodontitis.
• To elucidate the underlying mechanisms of SPRC's action, including its impact on H2S production and immune cell balance.

Main Methods:

• A rat model of periodontitis was induced using LPS.
• SPRC was administered at different doses (0, 25, 50 mg/kg/d).
• Levels of H2S, CSE, inflammatory factors (IL-17A, IL-6, TGF-β1, IL-10), Th17/Treg cells, and phosphorylated ERK1/2/CREB were assessed using various techniques including micro-CT, HE staining, RT-PCR, Western blot, and flow cytometry.

Main Results:

• SPRC administration increased gingival CSE expression and peripheral blood H2S concentration.
• SPRC significantly inhibited alveolar bone resorption.
• SPRC modulated inflammatory factors, downregulating IL-17A and upregulating IL-6 and TGF-β1.
• SPRC treatment promoted Treg cell differentiation and inhibited Th17 cell differentiation by suppressing ERK/CREB phosphorylation.

Conclusions:

• SPRC exhibits protective effects against periodontitis.
• SPRC exerts its therapeutic effects by enhancing endogenous H2S production.
• SPRC regulates the Th17/Treg balance via the ERK/CREB signaling pathway, offering a potential therapeutic strategy for periodontitis.