板蓝根F_(022)部位抗内毒素分子机理研究  

Studies on the Anti-endotoxic Molecular Mechanism of F_(022) from Radix Isatidis

作　　者：林爱华 刘云海[2] 刘奕明 

机构地区：[1]广州中医药大学第二附属医院,广东广州510120 [2]华中科技大学同济医学院附属同济医院,湖北武汉430030

出　　处：《时珍国医国药》2006年第6期897-899,共3页Lishizhen Medicine and Materia Medica Research

基　　金：国家自然科学基金资助项目(No.39870872)

摘　　要：目的探讨板蓝根F022部位抗内毒素分子机理。方法内毒素定量检测法测定F022样品液对内毒素的破坏作用;研究样品液对内毒素致鼠巨噬细胞分泌炎性因子的抑制作用、对蛋白激酶MAPKp38活性的影响、对内毒素刺激鼠组织moesin mRNA分子表达及对内毒素诱导鼠体内TNF-,αIL-6和NO的抑制作用。结果1%F022对内毒素破坏率达到86.5%,F022能显著抑制内毒素刺激巨噬细胞分泌TNF-,αIL-6水平;抑制内毒素刺激蛋白激酶MAPKp38活性;降低内毒素刺激鼠肝、肾、脾组织moesin mRNA和体内TNF-,αIL-6和NO等炎性因子的表达。结论F022部位不仅直接破坏内毒素结构,且阻断内毒素引起的信号传导通路,从而抑制机体炎性因子的过度释放、抑制膜结构伸展刺突蛋白和丝裂原活化蛋白激酶的表达,从分子水平阐明了板蓝根中活性部位F022抗内毒素的分子机理。Objective To study the anti - endotoxic molecular mechanism of F002 from Radix lsatidis. Methods The content of F022-pretreated ET was quantitatively determined with limulus test. The inhibition of TNF-α and IL-6 of murine peritoneal macrophages stimulated by LPS, the molecular expression of moesin mRNA, MAPK p38, TNF-α, IL-6 and NO in mice tissues induced by LPS were studied on the antiendotoxic mechanism of F002. Results It was found that the ET reduction rate was 86.5%, if 1% F022was added to macrophages culture before addition of 50 ng · ml^-1 LPS. Production of TNF-α, IL-6 and MAPKp38 by macrophages were inhibited in vitro. F022 remarkably decreased the molecular expression of moesin mRNA in liver, kidney, spleen induced by LPS in mice and inhibited production of TNF-α, IL-6 and NO in mice stimulated by LPS. Conclusion F002 from Radix lsatidis can not only destroy the structure of endotoxin, but also obstruct the signal transduction pathways of LPS. F002 may be a strong anti-endotoxin fraction in drugs research and development.

关 键 词：板蓝根 F002部位 内毒素 分子机理 

分 类 号：R285.5[医药卫生—中药学]