一种新的细胞因子：甲硫氨酸脑啡肽的可能作用途径。
A new cytokine: the possible effect pathway of methionine enkephalin.
作者信息
Liu Xin-Hua, Huang Dong-Ai, Yang Fei-Yi, Hao Yan-Sheng, Du Guo-Guang, Li Ping-Feng, Li Gang
机构信息
Department of Biochemistry and Molecular Biology, Health Science Center, Peking University, Beijing 100083, China.
出版信息
World J Gastroenterol. 2003 Jan;9(1):169-73. doi: 10.3748/wjg.v9.i1.169.
AIM
To investigate experimentally the effects of methionine enkephalin on signal transduction of mouse myeloma NS-1 cells.
METHODS
The antigen determinate of delta opioid receptor was designed in this lab and the polypeptide fragment of antigen determinate with 12 amino acids residues was synthesized. Monoclonal antibody against this peptide fragment was prepared. Proliferation of Mouse NS-1 cells treated with methionine enkephalin of 1 x 10(-6) mol x L(-1) was observed. The activities of protein kinase A (PKA) and protein kinase C (PKC) were measured and thereby the mechanism of effect of methionine enkephalin was postulated.
RESULTS
The results demonstrated that methionine enkephalin could enhance the proliferation of NS-1 cells and the effect of methionine enkephalin could be particularly blocked by monoclonal antibody. The activity of PKA was increased in both cytosol and cell membrane. With reference to PKC, the intracellular activity of PKC in NS-1 cells was elevated at 1 x 10(-7) mol x L(-1) and then declined gradually as the concentration of methionine enkephalin was raised. The effects of methionine enkephalin might be reversed by both naloxone and monoclonal antibody.
CONCLUSION
Coupled with the findings, it indicates that the signal transduction systems via PKA and PKC are involved in the effects of methionine enkephalin by binding with the traditional opioid receptors,and therefore resulting in different biological effects.
目的
通过实验研究甲硫氨酸脑啡肽对小鼠骨髓瘤NS-1细胞信号转导的影响。
方法
本实验室设计了δ阿片受体的抗原决定簇，合成了具有12个氨基酸残基的抗原决定簇多肽片段。制备了针对该肽片段的单克隆抗体。观察用1×10⁻⁶ mol·L⁻¹甲硫氨酸脑啡肽处理的小鼠NS-1细胞的增殖情况。测定蛋白激酶A（PKA）和蛋白激酶C（PKC）的活性，从而推测甲硫氨酸脑啡肽的作用机制。
结果
结果表明，甲硫氨酸脑啡肽可增强NS-1细胞的增殖，且甲硫氨酸脑啡肽的作用可被单克隆抗体特异性阻断。PKA在细胞质和细胞膜中的活性均增加。对于PKC，NS-1细胞内PKC的活性在1×10⁻⁷ mol·L⁻¹时升高，然后随着甲硫氨酸脑啡肽浓度的升高而逐渐下降。甲硫氨酸脑啡肽的作用可被纳洛酮和单克隆抗体逆转。
结论
结合研究结果表明，通过与传统阿片受体结合，经由PKA和PKC的信号转导系统参与了甲硫氨酸脑啡肽的作用，从而产生不同的生物学效应。
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