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Effects of rutin on the oxidative stress, proliferation and osteogenic differentiation of periodontal ligament stem cells in LPS-induced inflammatory environment and the underlying mechanism.
Journal of Molecular Histology ( IF 3.2 ) Pub Date : 2020-03-28 , DOI: 10.1007/s10735-020-09866-9
Bin Zhao 1, 2, 3 , Wenjing Zhang 1, 2, 3 , Yixuan Xiong 1, 2, 3 , Yunpeng Zhang 1, 2, 3, 4 , Dongjiao Zhang 1, 2, 3 , Xin Xu 1, 2, 3
Affiliation  

Periodontitis can cause damage to dental support tissue and affect the function of periodontal ligament cells. Rutin, a common flavonoid, plays a key role in anti-inflammatory responses, tissue repair and bone development. The purpose of this study was to investigate the effects of rutin on the oxidative stress, proliferation, and osteogenic differentiation of human periodontal ligament stem cells (PDLSCs) in an inflammatory environment and the underlying mechanism. Lipopolysaccharide (LPS) was used to stimulate PDLSCs to mimic an inflammatory environment model. Reactive oxygen species (ROS) levels were detected by the dichlorodihydrofluorescein diacetate (DCFH-DA) probe and the oxidative stress factors were tested by an oxidative stress factor detection kit. Moreover, the proliferation of PDLSCs was evaluated by cell counting kit-8 (CCK-8) assay. In addition, the osteogenic differentiation of PDLSCs was determined by alkaline phosphatase (ALP) staining, ALP activity test, alizarin red staining, and alizarin red semi-quantitative analysis. Furthermore, the protein levels of AKT and p-AKT were detected by Western blot. The results showed that rutin inhibited the release of ROS and increased the secretion of oxidative stress factors [superoxide dismutase (SOD) and glutathione (GSH)] and promoted the proliferation of PDLSCs in an inflammatory environment. Moreover, rutin upregulated ALP activity and enhanced the number of mineralized nodules. Conversely, the use of LY294002 (an inhibitor of PI3K) blocked the activation of the PI3K/AKT signaling pathway and prevented the beneficial effects of rutin. In conclusion, rutin promoted the antioxidative stress ability, proliferation and osteogenic differentiation of PDLSCs through PI3K/AKT signaling pathway in LPS-induced inflammatory environment.

中文翻译:

芦丁对LPS诱导的炎症环境中牙周膜干细胞氧化应激,增殖和成骨分化的影响及其潜在机制。

牙周炎可导致牙齿支持组织受损并影响牙周膜细胞的功能。芦丁是一种常见的类黄酮,在抗炎反应,组织修复和骨骼发育中起关键作用。本研究的目的是研究芦丁在炎性环境中对人牙周膜干细胞(PDLSC)的氧化应激,增殖和成骨分化的影响及其潜在机制。脂多糖(LPS)用于刺激PDLSCs模仿炎症环境模型。用二乙酸二氯二氢荧光素(DCFH-DA)探针检测活性氧(ROS)的水平,并通过氧化应激因子检测试剂盒测试氧化应激因子。此外,通过细胞计数试剂盒8(CCK-8)分析评估了PDLSCs的增殖。此外,通过碱性磷酸酶(ALP)染色,ALP活性测试,茜素红染色和茜素红半定量分析确定了PDLSCs的成骨分化。此外,通过蛋白质印迹检测AKT和p-AKT的蛋白质水平。结果表明,芦丁抑制了ROS的释放,并增加了氧化应激因子[超氧化物歧化酶(SOD)和谷胱甘肽(GSH)]的分泌,并促进了PDLSCs在炎性环境中的增殖。此外,芦丁上调了ALP活性并增加了矿化的结节数量。相反,LY294002(PI3K抑制剂)的使用阻止了PI3K / AKT信号通路的激活,并阻止了芦丁的有益作用。总之,芦丁具有增强抗氧化应激能力,
更新日期:2020-03-28
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