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儿茶素抑制人牙髓细胞中血管内皮生长因子的产生和环氧合酶-2的表达。

Catechins inhibit vascular endothelial growth factor production and cyclooxygenase-2 expression in human dental pulp cells.

作者信息

Nakanishi T, Mukai K, Hosokawa Y, Takegawa D, Matsuo T

机构信息

Department of Conservative Dentistry, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.

出版信息

Int Endod J. 2015 Mar;48(3):277-82. doi: 10.1111/iej.12312. Epub 2014 Jun 25.

Abstract

AIM

To investigate the effect of catechins on vascular endothelial growth factor (VEGF) production and cyclooxygenase-2 (COX-2) expression in human dental pulp cells (HDPC) stimulated with bacteria-derived factors or pro-inflammatory cytokines.

METHODOLOGY

Morphologically fibroblastic cells established from explant cultures of healthy human dental pulp tissues were used as HDPC. HDPC pre-treated with catechins, epigallocatechin-3-gallate (EGCG) or epicatechin gallate (ECG), were exposed to lipopolysaccharide (LPS), peptidoglycan (PG), interlukin-1β (IL-1β) or tumour necrosis factor-α (TNF-α). VEGF production was examined by enzyme-linked immunosorbent assay, and COX-2 expression was assessed by immunoblot.

RESULTS

EGCG and ECG significantly reduced LPS- or PG-mediated VEGF production in the HDPC in a dose-dependent manner. EGCG also prevented IL-1β-mediated VEGF production. Although TNF-α did not enhance VEGF production in the dental pulp cells, treatment of 20 μg mL(-1) of EGCG decreased the level of VEGF. In addition, the catechins attenuated COX-2 expression induced by LPS and IL-1β.

CONCLUSIONS

The up-regulated VEGF and COX-2 expressions in the HDPC stimulated with these bacteria-derived factors or IL-1β were diminished by the treatment of EGCG and ECG. These findings suggest that the catechins may be beneficial as an anti-inflammatory tool of the treatment for pulpal inflammation.

摘要

目的

研究儿茶素对细菌衍生因子或促炎细胞因子刺激的人牙髓细胞(HDPC)中血管内皮生长因子(VEGF)生成及环氧合酶-2(COX-2)表达的影响。

方法

从健康人牙髓组织外植体培养建立的形态成纤维样细胞用作HDPC。用儿茶素、表没食子儿茶素-3-没食子酸酯(EGCG)或表儿茶素没食子酸酯(ECG)预处理的HDPC,暴露于脂多糖(LPS)、肽聚糖(PG)、白细胞介素-1β(IL-1β)或肿瘤坏死因子-α(TNF-α)。通过酶联免疫吸附测定法检测VEGF生成,通过免疫印迹评估COX-2表达。

结果

EGCG和ECG以剂量依赖性方式显著降低HDPC中LPS或PG介导的VEGF生成。EGCG还可阻止IL-1β介导的VEGF生成。尽管TNF-α未增强牙髓细胞中的VEGF生成,但20μg/mL的EGCG处理可降低VEGF水平。此外,儿茶素减弱了LPS和IL-1β诱导的COX-2表达。

结论

用EGCG和ECG处理可减少这些细菌衍生因子或IL-1β刺激的HDPC中上调的VEGF和COX-2表达。这些发现表明,儿茶素作为牙髓炎症治疗的抗炎工具可能有益。

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