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骨髓间充质干细胞抑制脂多糖诱导的巨噬细胞和内皮细胞炎症反应。

Bone Marrow Mesenchymal Stem Cells Inhibit Lipopolysaccharide-Induced Inflammatory Reactions in Macrophages and Endothelial Cells.

作者信息

Li Dequan, Wang Cong, Chi Chuang, Wang Yuanyuan, Zhao Jing, Fang Jun, Pan Jingye

机构信息

Department of Traumatology Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China.

School of Pharmacy, Wenzhou Medical University, Wenzhou, Zhejiang 325000, China.

出版信息

Mediators Inflamm. 2016;2016:2631439. doi: 10.1155/2016/2631439. Epub 2016 Jan 26.

Abstract

BACKGROUND

Systemic inflammatory response syndrome (SIRS) accompanied by trauma can lead to multiple organ dysfunction syndrome (MODS) and even death. Early inhibition of the inflammation is necessary for damage control. Bone marrow mesenchymal stem cells (BMSCs), as a novel therapy modality, have been shown to reduce inflammatory responses in human and animal models.

METHODS

In this study, we used Western blot, quantitative PCR, and enzyme-linked immunosorbent assay (ELISA) to assess the activity of BMSCs to suppress the inflammation induced by lipopolysaccharide (LPS) in human umbilical cord endothelial cells (HUVECs) and alveolar macrophages.

RESULTS

Our results demonstrated that LPS caused an inflammatory response in alveolar macrophages and HUVECs, increased permeability of HUVEC, upregulated expression of toll-like receptor (TLR) 2, TLR4, phosphorylated p65, downregulated release of IL10, and promoted release of TNF-α in both cells. Coculture with BMSCs attenuated all of these activities induced by LPS in the two tested cell types.

CONCLUSIONS

Together, our results demonstrate that BMSCs dosage dependently attenuates the inflammation damage of alveolar macrophages and HUVECs induced by LPS.

摘要

背景

伴有创伤的全身炎症反应综合征(SIRS)可导致多器官功能障碍综合征(MODS)甚至死亡。早期抑制炎症对于控制损伤至关重要。骨髓间充质干细胞(BMSCs)作为一种新型治疗方式,已被证明可在人和动物模型中减轻炎症反应。

方法

在本研究中,我们使用蛋白质印迹法、定量聚合酶链反应和酶联免疫吸附测定(ELISA)来评估BMSCs抑制人脐静脉内皮细胞(HUVECs)和肺泡巨噬细胞中脂多糖(LPS)诱导的炎症的活性。

结果

我们的结果表明,LPS在肺泡巨噬细胞和HUVECs中引起炎症反应,增加HUVEC的通透性,上调Toll样受体(TLR)2、TLR4、磷酸化p65的表达,下调IL10的释放,并促进两种细胞中TNF-α的释放。与BMSCs共培养减弱了LPS在两种受试细胞类型中诱导的所有这些活性。

结论

总之,我们的结果表明,BMSCs剂量依赖性地减轻LPS诱导的肺泡巨噬细胞和HUVECs的炎症损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a492/4746395/5f4018a0048e/MI2016-2631439.001.jpg

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