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葡萄籽原花青素可改善 2,4-二硝基氟苯(DNFB)诱导的接触性过敏反应,并抑制体外 T 细胞增殖。

Grape-seed proanthocyanidins ameliorate contact hypersensitivity induced by 2,4-dinitrofluorobenzene (DNFB) and inhibit T cell proliferation in vitro.

机构信息

Department of Toxicology, School of Public Health, Peking University, Beijing 100191, People's Republic of China.

出版信息

Toxicol Lett. 2012 Apr 5;210(1):1-8. doi: 10.1016/j.toxlet.2012.01.009. Epub 2012 Jan 18.

Abstract

Contact hypersensitivity (CHS) is a delayed-type hypersensitivity reaction which is mediated by hapten-specific T cells. Strong haptens, such as 2, 4-dinitrofluorobenzene (DNFB) can induce it. Grape seed proanthocyanidins extract (GSPs), which is an antioxidant derived from grape seeds, has been reported to possess a variety of potent properties. However, few reports demonstrated the effects of GSPs on contact hypersensitivity. Therefore, the present study was devised to describe the role of GSPs on a mouse model of experimental CHS induced by DNFB and try to explore the possible underlying mechanisms. We observed that, GSPs when orally administrated into the CHS mice, inhibited the aggravation of inflammation. After administration of GSPs, there was obvious fewer inflammatory cell infiltration in the inflamed ears. Ear swelling after challenge was significantly reduced. In addition, we investigated the effects of GSPs on T cells in vitro, which play critical role during the progress of CHS. It was found that GSPs inhibited proliferative activity of T cells by blocking the activation of mitogen-activated protein kinases (MAPK) and NF-кB signaling pathways. Collectively, these results showed that GSPs has protective effect on CHS induced by DNFB and it also could inhibit the proliferation ability of T cells in vitro, suggesting the potential of GSPs as new and effective compound for the treatment of T-cell mediated inflammatory diseases.

摘要

接触超敏反应(CHS)是一种迟发型超敏反应,由半抗原特异性 T 细胞介导。强半抗原,如 2,4-二硝基氟苯(DNFB),可以诱导其发生。葡萄籽原花青素提取物(GSPs)是一种源自葡萄籽的抗氧化剂,已被报道具有多种强效特性。然而,很少有报道表明 GSPs 对接触超敏反应的影响。因此,本研究旨在描述 GSPs 在 DNFB 诱导的实验性 CHS 小鼠模型中的作用,并试图探索其可能的潜在机制。我们观察到,GSPs 在口服给予 CHS 小鼠时,抑制了炎症的加重。给予 GSPs 后,发炎的耳朵中炎症细胞浸润明显减少。挑战后的耳部肿胀明显减轻。此外,我们研究了 GSPs 对体外 T 细胞的作用,T 细胞在 CHS 进展过程中发挥关键作用。结果发现,GSPs 通过阻断丝裂原活化蛋白激酶(MAPK)和 NF-кB 信号通路的激活,抑制 T 细胞的增殖活性。综上所述,这些结果表明 GSPs 对 DNFB 诱导的 CHS 具有保护作用,并且还可以抑制体外 T 细胞的增殖能力,表明 GSPs 作为一种新的、有效的 T 细胞介导的炎症性疾病治疗化合物具有潜力。

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