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血小板衍生生长因子调节炎症性关节疾病下滑膜细胞细胞因子的分泌。

Platelet-Released Growth Factors Modulate the Secretion of Cytokines in Synoviocytes under Inflammatory Joint Disease.

机构信息

Institute of Anatomy and Cell Biology, Medical Faculty, RWTH Aachen University, Wendlingweg 2, 52074 Aachen, Germany.

Department of Heart and Vascular Surgery, University Hospital of Schleswig-Holstein, Kiel, Germany.

出版信息

Mediators Inflamm. 2017;2017:1046438. doi: 10.1155/2017/1046438. Epub 2017 Nov 19.

Abstract

The etiology and pathogenesis of rheumatoid arthritis (RA) are marked by a complex interplay of various cell populations and is mediated by different signaling pathways. Traditionally, therapies have primarily focused on pain relief, reducing inflammation and the recovery of joint function. More recently, however, researchers have discussed the therapeutic efficacy of autologous platelet-rich plasma (PRP). The main objective of this work is to examine the influences of platelet-released growth factor (PRGF) on human synoviocytes under inflammatory conditions. Additionally, it is checked to which extend treatment with platelet concentrate influences the release of cytokines form synoviocytes. For this purpose, an in vitro RA model was created by stimulating the cells with the TNF-. The release of cytokines was measured by ELISA. The cytokine gene expression was analyzed by real-time PCR. It has been observed that the stimulation concentration of 10 ng/ml TNF- resulted in a significantly increased endogenous secretion and gene expression of IL-6 and TNF-. The anti-inflammatory effect of PRGF could be confirmed through significant reduction of TNF- and IL-1. An induced inflammatory condition seems to cause PRGF to inhibit the release of proinflammatory cytokines. Further study is required to understand the exact effect mechanism of PRGF on synoviocytes.

摘要

类风湿关节炎(RA)的病因和发病机制以各种细胞群体的复杂相互作用为特征,并由不同的信号通路介导。传统上,治疗主要集中在缓解疼痛、减轻炎症和恢复关节功能上。然而,最近研究人员已经讨论了自体富血小板血浆(PRP)的治疗效果。这项工作的主要目的是研究血小板释放的生长因子(PRGF)在炎症条件下对人滑膜细胞的影响。此外,还检查了血小板浓缩物治疗对滑膜细胞释放细胞因子的影响程度。为此,通过用 TNF-刺激细胞来创建体外 RA 模型。通过 ELISA 测量细胞因子的释放。通过实时 PCR 分析细胞因子基因表达。已经观察到,刺激浓度为 10ng/ml TNF-导致内源性 IL-6 和 TNF-的分泌和基因表达显著增加。PRGF 的抗炎作用可以通过 TNF-和 IL-1 的显著减少得到证实。诱导的炎症状态似乎导致 PRGF 抑制促炎细胞因子的释放。需要进一步研究来了解 PRGF 对滑膜细胞的确切作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28bd/5733972/d94c5744bb76/MI2017-1046438.001.jpg

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