Kim Seung Hyun, Kim Tae Sung, Kim Sung Jun, Seong Chi Nam, Lee Oh Hyung, Lee Hyo Jung, Yoo Jin Cheol
School of Life Sciences and Biotechnology, Korea University, Seoul, Korea.
Immunopharmacol Immunotoxicol. 2007;29(1):131-9. doi: 10.1080/08923970701283476.
Pharmacological inhibition of interleukin-12 (IL-12) production may be a therapeutic strategy for preventing development and progression of disease in experimental models of autoimmunity. The acetone fraction prepared from bamboo, Phyllostachys nigra var. henonis, potently inhibited the Lipo polysaccharide (LPS)-induced IL-12 production from RAW264.7 monocytic cell-line in a dose-dependent manner. The repressive effect mapped to a region in the IL-12 gene promoter containing a binding site for NF-kappaB. Furthermore, activation of macrophages by LPS resulted in markedly enhanced binding activity to the NF-kappaB site, which significantly decreased upon addition of the acetone fraction of Phyllostachys nigra var. henonis. This indicated that the acetone fraction inhibited IL-12 production in LPS-activated macrophages via inhibition of NF-kappaB binding activity.
对白介素-12（IL-12）产生进行药理抑制可能是在自身免疫性疾病实验模型中预防疾病发生和发展的一种治疗策略。从毛竹（Phyllostachys nigra var. henonis）制备的丙酮提取物以剂量依赖性方式强烈抑制脂多糖（LPS）诱导的RAW264.7单核细胞系中IL-12的产生。这种抑制作用定位于IL-12基因启动子中包含核因子κB（NF-κB）结合位点的区域。此外，LPS激活巨噬细胞导致与NF-κB位点的结合活性显著增强，而添加毛竹丙酮提取物后这种活性明显降低。这表明丙酮提取物通过抑制NF-κB结合活性来抑制LPS激活的巨噬细胞中IL-12的产生。
