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[牡荆素对脂多糖诱导的牙髓干细胞中炎性细胞因子表达的影响]

[Influence of vitexin on the expression of inflammatory cytokines in dental pulp stem cells induced by lipopolysaccharide].

作者信息

Niu Chen-Guang, Li Jia-Yang, Yu Li-Ming, Chen Dong, Wei Xiao-Ling

机构信息

Oral Biomedical Engineering Laboratory, Shanghai Stomatological Hospital, Fudan University. Shanghai 200001, China. E-mail:

出版信息

Shanghai Kou Qiang Yi Xue. 2020 Oct;29(5):462-465.

Abstract

PURPOSE

To investigate the effect of vitexin (VTX) on the expression of inflammatory cytokines in human dental pulp stem cells(hDPSCs) induced by lipopolysaccharide(LPS), and to explore the underlying mechanism.

METHODS

hDPSCs were isolated and cultured, and CCK-8 method was used to detect the effect of VTX on proliferation of hDPSCs. hDPSCs were randomly divided into 4 groups: blank group (without LPS and VTX),LPS group (2 μg/mL LPS),2 μg/mL LPS + 25 μmol/L VTX,2 μg/mL LPS + 50 μmol/L VTX. The cells of all groups were cultured for 48 h. The gene levels of IL-1β, IL-6 and IL-8 in hDPSCs were detected by real time qPCR(RT-qPCR). The change of COX-2 and MAPKs signaling pathways were detected by Western blot. SPSS 16.0 software package was used for statistical analysis.

RESULTS

When the VTX concentration was less than 200 μmol/L, the cell viability was not affected(P>0.05). VTX at 25 and 50 μmol/L significantly reduced LPS-induced expression of IL-1β, IL-6 and IL-8 at gene levels and COX-2 at protein level (P<0.05).

CONCLUSIONS

VTX significantly inhibited the activation of ERK and p38 signaling pathway. VTX can reduce LPS-induced inflammatory cytokine expression in hDPSCs via restraining the activation of ERK and p38 signaling pathway.

摘要

目的

研究牡荆素(VTX)对脂多糖(LPS)诱导的人牙髓干细胞(hDPSCs)中炎性细胞因子表达的影响,并探讨其潜在机制。

方法

分离培养hDPSCs,采用CCK-8法检测VTX对hDPSCs增殖的影响。将hDPSCs随机分为4组:空白组(无LPS和VTX)、LPS组(2 μg/mL LPS)、2 μg/mL LPS + 25 μmol/L VTX组、2 μg/mL LPS + 50 μmol/L VTX组。各组细胞培养48 h。采用实时定量PCR(RT-qPCR)检测hDPSCs中IL-1β、IL-6和IL-8的基因水平。采用蛋白质印迹法检测COX-2和MAPKs信号通路的变化。使用SPSS 16.0软件包进行统计分析。

结果

当VTX浓度小于200 μmol/L时,细胞活力不受影响(P>0.05)。25和50 μmol/L的VTX显著降低LPS诱导的基因水平上IL-1β、IL-6和IL-8的表达以及蛋白质水平上COX-2的表达(P<0.05)。

结论

VTX显著抑制ERK和p38信号通路的激活。VTX可通过抑制ERK和p38信号通路的激活来降低LPS诱导的hDPSCs中炎性细胞因子的表达。

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