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肌酸激酶脑型同工酶刺激丝裂原活化蛋白激酶,但抑制淋巴细胞中脂多糖诱导的γ干扰素。

CKBM stimulates MAPKs but inhibits LPS-induced IFN-gamma in lymphocytes.

作者信息

Chan Anthony S L, Yip Eric C H, Yung Lisa Y, Pang Haihong, Luk Sharon C W, Pang Shiu F, Wong Yung H

机构信息

Department of Biochemistry, the Molecular Neuroscience Center, and the Biotechnology Research Institute, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong, China.

出版信息

Phytother Res. 2006 Sep;20(9):725-31. doi: 10.1002/ptr.1943.

Abstract

CKBM is an herbal formula composed of five Chinese medicinal herbs (Panax ginseng, Schisandra chinensis, Fructus crataegi, Ziziphus jujuba and Glycine max) supplemented with processed Saccharomyces cerevisiae. It has been demonstrated that CKBM is capable of triggering the release of IL-6 and TNFalpha from human peripheral blood mononuclear cells. In this report, T-lymphocytic Sup-T1 cells and B-lymphocytic Ramos cells were utilized as cellular models to investigate how CKBM regulates intracellular signaling as well as the production of cytokines. CKBM stimulated the three major subgroups of mitogen-activated protein kinase (i.e. ERK, JNK and p38) in Sup-T1 cells, but only triggered the activation of ERK and p38 in Ramos cells. The induction of mitogen-activated protein kinases (MAPK) activations varied with the duration of treatment, as well as with the dosage of CKBM. In terms of cytokine production, treatment of CKBM alone did not trigger the release of IL-1beta and IFNgamma, but it suppressed the LPS-induced IFNgamma production from both Sup-T1 cells and Ramos cells. In view of the therapeutic effects of traditional Chinese medicines in inflammatory and autoimmune disorders, the results suggest that CKBM may exhibit its immuno-modulatory effects by regulating intracellular signaling as well as cytokine production in different lymphocytic cell types.

摘要

CKBM是一种草药配方,由五种中药(人参、五味子、山楂、枣和大豆)组成,并添加了经过加工的酿酒酵母。已经证明,CKBM能够触发人外周血单核细胞释放白细胞介素-6和肿瘤坏死因子α。在本报告中,T淋巴细胞Sup-T1细胞和B淋巴细胞Ramos细胞被用作细胞模型,以研究CKBM如何调节细胞内信号传导以及细胞因子的产生。CKBM刺激了Sup-T1细胞中丝裂原活化蛋白激酶的三个主要亚组(即ERK、JNK和p38),但仅触发了Ramos细胞中ERK和p38的激活。丝裂原活化蛋白激酶(MAPK)激活的诱导随治疗持续时间以及CKBM的剂量而变化。就细胞因子产生而言,单独使用CKBM处理不会触发白细胞介素-1β和干扰素γ的释放,但它抑制了脂多糖诱导的Sup-T1细胞和Ramos细胞中干扰素γ的产生。鉴于中药在炎症和自身免疫性疾病中的治疗作用,结果表明CKBM可能通过调节不同淋巴细胞类型中的细胞内信号传导以及细胞因子产生来发挥其免疫调节作用。

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