Abstract：
OBJECTIVE: 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.
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.
摘要：
目的：临床研究证实，牙周炎患者的半乳糖凝集素-3（Gal-3）水平显着升高。本研究旨在探讨Gal-3抑制对体外和体内牙周炎症的影响。
方法：脂多糖（LPS）刺激有或没有Gal-3敲低的人牙龈成纤维细胞（HGFs），并建立了用Gal-3抑制剂处理的结扎诱导的小鼠牙周炎模型。使用苏木精-伊红(H&E)和免疫组织化学(IHC)染色来评估牙龈组织中的Gal-3水平。采用实时定量聚合酶链反应(RT-PCR)和酶联免疫吸附试验(ELISA)检测Gal-3、白细胞介素(IL)-6、IL-8和C-C基序配体2(CCL2)的表达。免疫荧光和免疫印迹检测NF-κ5;B和ERK信号通路的激活。显微计算机断层扫描用于分析骨丢失的程度。
结果：Gal-3在发炎的牙龈组织和LPS诱导的HGF中显著上调。Gal-3敲低显著降低LPS诱导的IL-6、IL-8和CCL2表达,并阻断NF-κ5；B和ERK信号通路在HGFs中的激活。在小鼠牙周炎模型中,Gal-3抑制可显着减轻牙龈组织中IL-1β和IL-6的浸润，并减轻牙周骨丢失。
结论：Gal-3抑制作用通过阻断NF-κ5、B和ERK信号通路的激活而显著减轻牙周炎症。
方法：脂多糖（LPS）刺激有或没有Gal-3敲低的人牙龈成纤维细胞（HGFs），并建立了用Gal-3抑制剂处理的结扎诱导的小鼠牙周炎模型。使用苏木精-伊红(H&E)和免疫组织化学(IHC)染色来评估牙龈组织中的Gal-3水平。采用实时定量聚合酶链反应(RT-PCR)和酶联免疫吸附试验(ELISA)检测Gal-3、白细胞介素(IL)-6、IL-8和C-C基序配体2(CCL2)的表达。免疫荧光和免疫印迹检测NF-κ5;B和ERK信号通路的激活。显微计算机断层扫描用于分析骨丢失的程度。
结果：Gal-3在发炎的牙龈组织和LPS诱导的HGF中显著上调。Gal-3敲低显著降低LPS诱导的IL-6、IL-8和CCL2表达,并阻断NF-κ5；B和ERK信号通路在HGFs中的激活。在小鼠牙周炎模型中,Gal-3抑制可显着减轻牙龈组织中IL-1β和IL-6的浸润，并减轻牙周骨丢失。
结论：Gal-3抑制作用通过阻断NF-κ5、B和ERK信号通路的激活而显著减轻牙周炎症。
