2. Academic Validation
  3. D-aspartic acid protects against gingival fibroblasts inflammation by suppressing pyroptosis

D-aspartic acid protects against gingival fibroblasts inflammation by suppressing pyroptosis

  • Mol Biol Rep. 2022 Jul;49(7):5821-5829. doi: 10.1007/s11033-022-07335-y.
Xuechun Du # 1 2,  Baosheng Li # 1,  Qing Cai 1,  Shuwei Qiao 1 2,  Zixuan Wang 1 2,  Zhen Li 1 2,  Yuyang Li 1 3,  Weiyan Meng 4
Affiliations

Affiliations

  • 1 Department of Dental Implantology, Hospital of Stomatology, Jilin University, 130021, Changchun, Jilin, China.
  • 2 Jilin Provincial Key Laboratory of Tooth Development and Bone Remodeling, Changchun, Jilin, China.
  • 3 Department of Cariology and Endodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, Jiangsu, China.
  • 4 Department of Dental Implantology, Hospital of Stomatology, Jilin University, 130021, Changchun, Jilin, China. mengwy@jlu.edu.cn.
  • # Contributed equally.
PMID: 35716284 DOI: 10.1007/s11033-022-07335-y
Abstract

Background: Peri-implantitis is the main cause of dental implant failure, which is associated with Pyroptosis. The roles of D-aspartic acid (D-Asp) on Pyroptosis and the mechanism of the protective effect of D-Asp on human gingival fibroblasts (HGFs) remain unknown. This study investigated the effects of D-Asp on the Pyroptosis of HGFs induced by high mobility group box 1 protein (HMGB1).

Methods: The cytotoxic effects of D-Asp on HGFs was detected by Cell Counting Kit-8 assay, the membrane permeability was investigated by propidium iodide/ Hoechst 33,342 double staining, flow cytometry analysis, and Lactate Dehydrogenase releasing, The gene and protein expression levels were detected by real-time quantitative PCR, enzyme-linked immunosorbent assay, and Western blot, respectively.

Results: Cell viability analysis showed that D-Asp ≤ 30 mM had no cytotoxicity to HGFs. HMGB1 drastically raised the membrane permeability of HGFs, while 1/10/30 mM D-Asp suppressed the permeability and remained the integrity of the membrane. HMGB1 promoted the mRNA expression of NLRP3, Caspase-1, GSDMD, IL-1β, and IL-18, and the protein expression of IL-1β, IL-18, Caspase-1, GSDMD, and NLRP3.

Conclusions: With the pretreatment of HGFs with D-Asp of 1/10/30 mM for 24 h, the cell membrane permeability was reduced and the expression of NLRP3, Caspase-1, GSDMD, IL-1β, and IL-18 was significantly decreased compared with the HMGB1 group, indicating the competitive antagonism of D-Asp against HMGB1 on the binding with toll-like receptors. Hence, this study may provide a novel insight into preventing Pyroptosis and propose a new strategy for the treatment of peri-implantitis.

Keywords

D-aspartic acid; Fibroblast; HMGB1; Peri-implantitis; Pyroptosis.

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