首页> 外文期刊>The American Journal of Chinese Medicine >The Chloroform Fraction of Solanum nigrum Suppresses Nitric Oxide and Tumor Necrosis Factor-® in LPS-Stimulated Mouse Peritoneal Macrophages Through Inhibition of p38, JNK and ERK1/2
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The Chloroform Fraction of Solanum nigrum Suppresses Nitric Oxide and Tumor Necrosis Factor-® in LPS-Stimulated Mouse Peritoneal Macrophages Through Inhibition of p38, JNK and ERK1/2

机译:龙葵的氯仿级分通过抑制p38,JNK和ERK1 / 2抑制LPS刺激的小鼠腹膜巨噬细胞中的一氧化氮和肿瘤坏死因子

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Solanum nigrum L., commonly known as black nightshade, is used worldwide fornthe treatment of skin and mucosal ulcers, liver cirrhosis and edema. We aimed to determinenthe anti-inflammatory active fraction of S. nigrum by serial extractions. S. nigrum was firstnextracted with methanol, then fractionated with chloroform and water. The effects of S.nnigrum fractions, diosgenin and u0001-solanine on LPS/interferon-gamma-induced nitric oxiden(NO) and inducible NO synthase (iNOS), or LPS-induced tumor necrosis factor-u0001 (TNF-u0001)nand interleukin (IL)-6, in mouse peritoneal macrophages were determined. Western blottingnanalysis was used to detect LPS-induced phosphorylation of p38, JNK and ERK1/2. Thenchloroform fraction of S. nigrum was cytotoxic in a time and concentration dependentnmanner; however, the methanol and water fractions were not. The chloroform fractionnreduced NO through inhibition of iNOS synthesis and inhibited TNF-u0001 and IL-6 at the levelnof protein secretion; the methanol and water fractions showed a weak or no effect. Thenchloroform fraction also suppressed p38, JNK and ERK1/2. Diosgenin and u0001-solanine werencytotoxic at a high concentration. In particular, diosgenin was able to inhibit TNF-u0001 andnIL-6, but both compounds did not affect LPS-induced iNOS expression. These resultsnindicate that the anti-inflammatory compounds of S. nigrum exist preferentially in thennonpolar fraction, ruling out the possibility that diosgenin and u0001-solanine are the likelyncandidates. The inhibition of iNOS, TNF-u0001 and IL-6 by the chloroform fraction may benCorrespondence to: Dr. Ho-Young Choi, Department of Herbology, College of Oriental Medicine, Kyung HeenUniversity, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, South Korea. Tel: (t82) 2-961-0323, Fax: (t82)n2-965-9372, E-mail: hychoi@khu.ac.krnThe American Journal of Chinese Medicine, Vol. 39, No. 6, 1261–1273n© 2011 World Scientific Publishing CompanynInstitute for Advanced Research in Asian Science and MedicinenDOI: 10.1142/S0192415X11009548n1261npartly due to the suppression of p38, JNK and ERK1/2. Further study is required to identifynthe active compounds of S. nigrum.
机译:龙葵(Solanum nigrum L.)通常被称为黑色茄属植物,在全世界范围内被用于治疗皮肤和粘膜溃疡,肝硬化和水肿。我们旨在通过连续提取来确定黑链霉菌的抗炎活性部分。首先用甲醇将黑葡萄球菌提取,然后用氯仿和水分级分离。链球菌级分,薯os皂素和u0001-茄碱对LPS /干扰素-γ诱导的一氧化氮(NO)和诱导型NO合酶(iNOS)或LPS诱导的肿瘤坏死因子-u0001(TNF-u0001)n和白介素的影响(IL)-6,在小鼠腹膜巨噬细胞中测定。 Western blottingnanalysis用于检测LPS诱导的p38,JNK和ERK1 / 2的磷酸化。然后,黑链霉菌的氯仿级分在一定时间和浓度下具有细胞毒性。但是,甲醇和水的馏分却没有。氯仿组分通过抑制iNOS的合成而减少NO,并在蛋白质分泌水平抑制TNF-u0001和IL-6。甲醇和水的馏分显示出微弱或无作用。然后氯仿组分也抑制了p38,JNK和ERK1 / 2。薯皂素和u0001-茄碱在高浓度下均具有细胞毒性。特别地,薯os皂苷元能够抑制TNF-u0001和nIL-6,但两种化合物均不影响LPS诱导的iNOS表达。这些结果表明,黑链霉菌的抗炎化合物优先存在于非极性组分中,排除了薯os皂苷元和u0001-茄碱是可能的念珠菌的可能性。氯仿组分对iNOS,TNF-u0001和IL-6的抑制作用可能对应于:首尔市东大门区会吉洞市庆熙大学东方医学院草药学系崔浩英博士130 -701,韩国。电话:(t82)2-961-0323,传真:(t82)n2-965-9372,电子邮件:hychoi@khu.ac.krn 39,第6号,1261-1273n©2011世界科学出版公司n亚洲科学和医学高级研究所nDOI:10.1142 / S0192415X11009548n1261n部分是由于抑制了p38,JNK和ERK1 / 2。需要进一步研究以鉴定黑链霉菌的活性化合物。

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