蛋氨酸—脑啡肽改变缺锌小鼠脾淋巴细胞的增殖反应

本试验检测蛋氨酸—脑啡肽(M—EnK)在缺锌(Zn)组、配对组和对照组小鼠脾细胞对促细胞分裂原和混合淋巴细胞培养(MLC)反应上的效应。试验数据显示M—EnK能抑制以上3组淋巴细胞对ConA的反应,但对缺Zn组的抑制作用较小。M—EnK也能增进所有各组对美洲商陆(PWM)以及减少对脂多糖(LPS)的反应。对ConA、PWM和LPS增殖反应的改变可以被10μmol/L纳络酮所逆转。提示M—EnK在细胞增殖反应上的效应是通过阿片受体介导而实现的。在MLC增殖反应中,在缺少M—EnK时,缺Zn小鼠淋巴细胞的反应增加,M—EnK能抑制这种增加的反应。试验结果表明M—EnK能改变有丝分裂反应方式,Zn缺乏又能影响这种改变。

METHIONINE-ENKEPHALIN ALTERATION OF MITOGENIC AND MIXED LYMPHOCYTE CULTURE RESPONSES IN ZINC-DEFICIENT MICE

The effects of methionine-enkephalin (M-EnK) on mitogenic and mixed lymphocyte culture (MLC) proliferation of splenocytes from Zn-deficient, restricted and control mice were evaluated. The data from this experiment showed that M-Enk could suppress the responses of splenocyte from th 3 groups to eoncanavalin A(Con A), but less inhibition was observed in the Zn-deficient group. M-Enk could also enhance the responses to Pokeweed Mitogen (PWM) and decrease the response to Lipopolysaceharide (LPS) in all groups. Alteration of proliferative responses to LPS,Con A and FWM was reversible in the presence of 10 μmol/L naloxone, indicating that the effect of M-Enk on cellular proliferation was mediated by the opioid receptor. In the proliferation of MLC, the response of lymphocytes from Zndeficient mice was increased in the absence of M-Enk and M-Enk could suppress this increased response. It is therefore concluded that Met-Enk can modify the pattern of mitogenic responses and the alteration in Con A and MLC responses can be influenced by zinc deficiency.