Anti-inflammatory effects of BT-201, an n-butanol extract of Panax notoginseng, observed in vitro and in a collagen-induced arthritis model
Anti-inflammatory effects of BT-201, an n-butanol extract of Panax notoginseng, observed in vitro and in a collagen-induced arthritis model
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DOI：
10.1016/j.clnu.2007.07.008
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发表时间：
2007-12-01
影响因子：
6.3
通讯作者：
Kim, Jung-Keun
中科院分区：
文献类型：
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作者：
Chang, Sun-Hwa;Choi, Youngnim;Kim, Jung-Keun
背景和目标：尽管基于蛋白质的抗肿瘤坏死因子α（TNF-α）疗法取得了一些成功，但与基于蛋白质的药物相关的问题需要替代方法。我们筛选了各种草药。研究人员发现三七提取物具有抑制 TNF-α 分泌的能力，并发现三七 (P. notoginseng) 的正丁醇提取物 BT-201 具有这种能力。 方法：本研究的目的是评估 BT-201 的抗炎和抗风湿作用。通过体外测量 BT-201 对 TNF-α、白细胞介素 (IL)-1 ss、诱导型一氧化氮 (iNO) 和基质金属蛋白酶-13 (MMP-13) 产生的影响来评估抗炎作用。通过每天口服 15 毫克/公斤/天的 BT-201 治疗患有胶原诱导关节炎 (CIA) 的小鼠来评估抗风湿作用。此外，使用磷酸特异性抗体通过蛋白质印迹评估了对 NF-kappa B 和丝裂原激活蛋白激酶 (MAPK) 通路的影响。结果：BT-201 显着抑制所有通路。体外评估的炎症参数延缓了 CIA 的发病和进展。 BT-201 抑制 NF-kappa B、ERK、p38 和 JNK 通路的激活。结论：我们的结果表明，BT-201 可以在体外调节炎症的各个方面，并且在体内具有缓解疾病、抗风湿的作用，这表明它可以成为当前治疗类风湿关节炎和其他炎症性疾病的抗 TNF-α 疗法的潜在替代品。 (C) 2007 Elsevier Ltd 和欧洲临床营养与代谢学会。版权所有。
Background & aims: Although there has been some success with protein-based anti-tumor necrosis factor alpha (TNF-alpha) therapeutics, the problems associated with protein-based drugs demand alternative approaches. We screened various herbal. extracts for their ability to inhibit TNF-alpha secretions and found that BT-201, an n-butanol extract of Panax notoginseng (Burk.) F. H. Chen (P. notoginseng) has such an ability.Methods: The purpose of this study has been to evaluate the anti-inflammatory and antirheumatic effects of BT-201. The anti-inflammatory effects were evaluated by measuring the effects of BT-201 on the production of TNF-alpha, interleukin (IL)-1 ss, inducible nitric oxide (iNO), and matrix metalloproteinase- 13 (MMP-13), in vitro. The anti-rheumatic effects were evaluated by treating mice with collagen-induced arthritis (CIA) using a daily oral administration of BT-201 at 15 mg/kg/day. In addition, the effects on NF-kappa B and mitogen-activated protein kinase (MAPK) pathways were evaluated by Western blotting using phospho-specific antibodies.Results: BT-201 significantly inhibited all. the inflammatory parameters evaluated in vitro and delayed the onset and progression of CIA. BT-201 inhibited the activation of NF-kappa B, ERK, p38, and JNK pathways.Conclusions: Our results demonstrated that BT-201 can modulate various aspects of inflammation in vitro and that it has disease-modifying, anti-rheumatic effects in vivo,suggesting that it can be a potential alternative to the current anti-TNF-alpha therapeutics for rheumatoid arthritis and other inflammatory disease. (C) 2007 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.