儿茶素通过抑制 NF-κB 通路的激活来减少脂多糖刺激的牙髓细胞中的炎症反应。

Catechins reduce inflammation in lipopolysaccharide-stimulated dental pulp cells by inhibiting activation of the NF-κB pathway.

机构信息

Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.

Clinical Research Center of Shaanxi Province for Dental and Maxillofacial Diseases, College of Stomatology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.

出版信息

Oral Dis. 2020 May;26(4):815-821. doi: 10.1111/odi.13290. Epub 2020 Feb 21.

DOI:10.1111/odi.13290

PMID:31999881

Abstract

AIM

To ascertain the anti-inflammation mechanism of catechins in lipopolysaccharide-treated human dental pulp cells (HDPCs).

METHODS

Expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 was measured using quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assays. The anti-inflammatory mechanism was explored by examining activation of nuclear factor-kappa B (NF-κB) signaling using qPCR, Western blotting, and immunofluorescence staining.

RESULTS

Human dental pulp cells proliferation was not affected by treatment with epigallocatechin (ECG) or epigallocatechin 3-gallate (EGCG). mRNA expression of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 was decreased significantly in ECG- and EGCG-treated HDPCs. Subsequently, the effects of ECG and EGCG upon activation of NF-κB signaling were evaluated by Western blotting and immunofluorescence staining. Expression of p-p65 protein in HDPCs treated with ECG, EGCG, or an NF-κB inhibitor (Bay 11-7082) was lower than that in HDPCs treated with lipopolysaccharide, data that were consistent with the location of p65 protein according to immunofluorescence staining.

CONCLUSIONS

Catechin could reduce lipopolysaccharide-stimulated inflammation in HDPCs by inhibiting activation of the NF-κB pathway.

摘要

目的

确定儿茶素在脂多糖处理的人牙髓细胞（HDPCs）中的抗炎机制。

方法

采用实时聚合酶链反应（qPCR）和酶联免疫吸附试验（ELISA）检测肿瘤坏死因子（TNF）-α、白细胞介素（IL）-1β和 IL-6 的表达。通过 qPCR、Western 印迹和免疫荧光染色检测核因子-κB（NF-κB）信号的激活，探讨抗炎机制。

结果

儿茶素（ECG）和表没食子儿茶素没食子酸酯（EGCG）处理对人牙髓细胞的增殖没有影响。ECG 和 EGCG 处理的 HDPCs 中促炎细胞因子 TNF-α、IL-1β 和 IL-6 的 mRNA 表达显著降低。随后，通过 Western 印迹和免疫荧光染色评估 ECG 和 EGCG 对 NF-κB 信号激活的影响。与 LPS 处理的 HDPCs 相比，ECG、EGCG 或 NF-κB 抑制剂（Bay 11-7082）处理的 HDPCs 中 p-p65 蛋白的表达较低，根据免疫荧光染色，这与 p65 蛋白的位置一致。