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

详细信息	查看全文 | 推荐本文 |

• 作者：Qiuqiong Tang ; Peng Zou ; Haifeng Jin ; Jun Fu ; Jintao Yang ; Lanqin Shang ; Xuetao Wei ; ^{Weixt@263.net}
• 关键词：CHS ; hypersensitivity ; Con A ; concanavalin A ; DNFB ; 2 ; 4-dinitrofluorobenzene ; DMSO ; dimethylsulfoxide ; MTT ; 3-(4 ; 5-dimethythiazol-2-yl)-2 ; 5-diphenyltetrazolium bromide ; PMA ; phorbol 12-myristate 13-acetate
• 刊名：Toxicology Letters
• 出版年：2012
• 期刊代码：49_03784274
• 类别：pha
• 出版时间：5 April, 2012
• 卷：210
• 期：1
• 页码：1-8
• 文件大小：1209 K

摘要

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-泻B 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.