Galectin-3 inhibition alleviated LPS-induced periodontal inflammation in gingival fibroblasts and experimental periodontitis mice.

IF 6.7 2区医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL

Clinical science Pub Date : 2024-06-19 DOI:10.1042/CS20240036

Song Wenjing, Liu Mengmeng, Shang Lingling, Ding Tian, Kang Wenyan, Ge Shaohua

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引用次数: 0

Abstract

Objectives: Clinical studies have confirmed that galectin-3 (Gal-3) levels are significantly elevated in periodontitis patients. The present study aimed to explore the effects of Gal-3 inhibition on periodontal inflammation in vitro and in vivo.

Methods: Human gingival fibroblasts (HGFs) with or without Gal-3 knockdown were stimulated by lipopolysaccharide (LPS), and a ligation-induced mouse periodontitis model treated with a Gal-3 inhibitor was established. Hematoxylin-eosin (H&E) and immunohistochemistry (IHC) staining were used to evaluate Gal-3 levels in gingival tissues. Quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were used to detect Gal-3, interleukin (IL)-6, IL-8, and C-C motif ligand 2 (CCL2) expression. Immunofluorescence and western blotting were used to detect NF-κB and ERK signaling pathway activation. Micro-computed tomography was used to analyse the degree of bone loss.

Results: Gal-3 was significantly up-regulated in inflamed gingival tissues and LPS-induced HGFs. Gal-3 knockdown markedly decreased LPS-induced IL-6, IL-8, and CCL2 expression and blocked NF-κB and ERK signaling pathway activation in HGFs. In the mouse periodontitis model, Gal-3 inhibition significantly alleviated IL-1β and IL-6 infiltration in gingival tissue and mitigated periodontal bone loss.

Conclusions: Gal-3 inhibition notably alleviated periodontal inflammation partly through blocking NF-κB and ERK signaling pathway activation.

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抑制 Galectin-3 可减轻 LPS 诱导的牙龈成纤维细胞和实验性牙周炎小鼠的牙周炎症。

目的：临床研究证实，牙周炎患者体内的galectin-3（Gal-3）水平显著升高。方法：用脂多糖（LPS）刺激敲除或未敲除 Gal-3 的人牙龈成纤维细胞（HGFs），并用 Gal-3 抑制剂建立结扎诱导的小鼠牙周炎模型。采用血红素-伊红（H&E）和免疫组化（IHC）染色法评估牙龈组织中的 Gal-3 水平。实时定量聚合酶链反应（ԛRT-PCR）和酶联免疫吸附试验（ELISA）用于检测 Gal-3、白细胞介素（IL）-6、IL-8 和 C-C motif ligand 2（CCL2）的表达。免疫荧光和 Western 印迹技术用于检测 NF-ᵰ5;B 和 ERK 信号通路的激活情况。显微计算机断层扫描用于分析骨质流失的程度：结果：在发炎的牙龈组织和 LPS 诱导的 HGFs 中，Gal-3 明显上调。结果：Gal-3在发炎的牙龈组织和LPS诱导的HGFs中明显上调，Gal-3敲除可明显降低LPS诱导的IL-6、IL-8和CCL2的表达，并阻断HGFs中NF-ᵰ5;B和ERK信号通路的激活。在小鼠牙周炎模型中，Gal-3抑制剂能显著缓解牙龈组织中IL-1β和IL-6的浸润，减轻牙周骨质流失：结论：Gal-3抑制剂通过阻断NF-ᵰ5;B和ERK信号通路的激活，明显减轻了牙周炎症。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Clinical science 医学-医学：研究与实验

CiteScore

11.40

自引率

0.00%

发文量

189

审稿时长

4-8 weeks

期刊介绍： Translating molecular bioscience and experimental research into medical insights, Clinical Science offers multi-disciplinary coverage and clinical perspectives to advance human health. Its international Editorial Board is charged with selecting peer-reviewed original papers of the highest scientific merit covering the broad spectrum of biomedical specialities including, although not exclusively: Cardiovascular system Cerebrovascular system Gastrointestinal tract and liver Genomic medicine Infection and immunity Inflammation Oncology Metabolism Endocrinology and nutrition Nephrology Circulation Respiratory system Vascular biology Molecular pathology.