Kim Jin-A, Kim Dae-Ki, Kang Ok-Hwa, Choi Yeon-A, Choi Suck-Chei, Kim Tae-Hyun, Nah Yong-Ho, Choi Suck-Jun, Kim Young-Ho, Bae Ki-Hwan, Lee Young-Mi
Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University, Iksan, Jeonbuk, 570-749, South Korea.
Clin Chim Acta. 2004 Apr;342(1-2):193-202. doi: 10.1016/j.cccn.2004.01.004.
Intestinal epithelial cells (IECs) can produce cytokines and chemokines that play an important role in the mucosal immune response. Regulation of this production is important to prevent inflammatory tissue damage. The root and stem barks of Acanthopanax species have been used as a tonic and sedative as well as in the treatment of rheumatism and diabetes. The aim of this study was to examine the inhibitory effect of acanthoic acid isolated from Acanthopanax koreanum (Araliaceae), on IL-8 production via mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-kappaB) in TNF-alpha-stimulated human colon epithelial cells.
HT29 cells were stimulated with TNF-alpha in the presence or absence of acanthoic acid. IL-8 production was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-PCR (RT-PCR). MAPK activation and IkappaB/NF-kappaB expression were assessed by Western blot analysis. NF-kappaB activation was determined using immunofluorescence localization and electrophoretic mobility shift assay (EMSA).
Acanthoic acid suppressed TNF-alpha-induced IL-8 production in a dose-dependent manner. Furthermore, acanthoic acid inhibited TNF-alpha-induced MAPKs (p38, JNK1/2, and ERK1/2) activation, IkappaB degradation, NF-kappaB nuclear translocation, and NF-kappaB/DNA binding activity.
Acanthoic acid might inhibit TNF-alpha-mediated IL-8 production by blocking in both the MAPKs and NF-kappaB pathways in HT29 cells.
肠上皮细胞（IECs）可产生细胞因子和趋化因子，它们在黏膜免疫反应中发挥重要作用。调节这种产生对于预防炎症性组织损伤很重要。刺五加属植物的根皮和茎皮已被用作滋补剂和镇静剂，还用于治疗风湿病和糖尿病。本研究的目的是检测从朝鲜刺五加（五加科）中分离得到的刺五加酸对肿瘤坏死因子-α（TNF-α）刺激的人结肠上皮细胞中白细胞介素-8（IL-8）通过丝裂原活化蛋白激酶（MAPKs）和核因子-κB（NF-κB）途径产生的抑制作用。
在有或没有刺五加酸存在的情况下，用TNF-α刺激HT29细胞。通过酶联免疫吸附测定（ELISA）和逆转录-聚合酶链反应（RT-PCR）测量IL-8的产生。通过蛋白质免疫印迹分析评估MAPK激活和IκB/NF-κB表达。使用免疫荧光定位和电泳迁移率变动分析（EMSA）确定NF-κB激活。
刺五加酸以剂量依赖性方式抑制TNF-α诱导的IL-8产生。此外，刺五加酸抑制TNF-α诱导的MAPKs（p38、JNK1/2和ERK1/2）激活、IκB降解、NF-κB核转位以及NF-κB/DNA结合活性。
刺五加酸可能通过阻断HT29细胞中的MAPKs和NF-κB途径来抑制TNF-α介导的IL-8产生。
