TRPV1 Promotes Periodontitis Tissue Inflammation and Oxidative Damage by Regulating STAT3 Signaling Pathway

氧化应激 炎症 TRPV1型 牙周炎 化学 细胞凋亡 信号转导 细胞生物学 癌症研究 免疫学 药理学 医学 生物 受体 内科学 生物化学 瞬时受体电位通道
作者
Mingzhu Yu,Huan Tian,Ruixiao Lu,Ni Quan,Ling Qian
出处
期刊:Journal of Periodontal Research [Wiley]
被引量:1
标识
DOI:10.1111/jre.13368
摘要

ABSTRACT Aims Periodontitis is a chronic disease affecting adult oral health. Transient receptor potential vanilloid 1 (TRPV1) expression is shown to upregulate in many inflammatory diseases. Nevertheless, its biological potential along with the molecular mechanism in periodontitis is unclear. Our study aimed to explore the biological role and underlying signaling pathway of TRPV1 in periodontitis. Methods In the current research, human periodontal ligament stem cells (hPDLSCs) were stimulated by lipopolysaccharide (LPS) to induce inflammatory conditions in vitro. In vivo, the periodontitis mouse model was built by ligating the gingival sulcus of male C57BL/6J mice. Thereafter, the proliferation, apoptosis, inflammation, and oxidative stress‐related processes were assessed. Results We found that LPS induced apoptosis and inflammation in hPDLCs, along with oxidative stress, while simultaneously inhibiting hPDLC proliferation ( p < 0.05). Notably, TRPV1 expression was elevated in LPS‐treated hPDLSCs and gingival samples from patients with periodontitis. Interestingly, the increase in TRPV1 expression induced by Capsaicin, a TRPV1 agonist, inhibited cell proliferation while promoting LPS‐stimulated apoptosis, inflammation, and oxidative stress in hPDLSCs ( p < 0.01). In contrast, inhibition of TRPV1 expression using Capsazepine, a TRPV1 inhibitor, produced opposite effects ( p < 0.01). In vivo experiments revealed that inhibition of TRPV1 attenuated ligation‐induced periodontitis in mice, as evidenced by enhanced oxidative stress, inflammatory response, and elevated apoptosis ( p < 0.01). Additionally, rescue assays indicated that TRPV1 promoted periodontitis‐associated tissue inflammation and oxidative damage via activating the STAT3 signaling pathway ( p < 0.01). Conclusion Our study demonstrates that TRPV1 expression is high in periodontitis and facilitates periodontitis‐associated tissue inflammation and oxidative damage by regulating STAT3 signaling pathway, which implies that TRPV1 may represent a new therapeutic target for periodontitis.
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