乙酰胆碱对大鼠体外抗体生成的影响

目的：观察不同浓度乙酰胆碱（ＡＣｈ，１０－１０～１０－５ｍｏｌ／Ｌ）对大鼠体外抗体生成的影响，并初步探讨其作用机制，从细胞水平了解乙酰胆碱与免疫功能之间的关系。方法：用体外抗体生成的检测方法，用绵羊红细胞（ＳＲＢＣ）刺激大鼠肠系膜淋巴结Ｂ细胞转化成抗体形成细胞（ＡＦＣ），然后检测其抗体生成量。结果：①１０－１０～１０－７ｍｏｌ／ＬＡＣｈ能显著抑制体外抗体生成，其中１０－８和１０－７ｍｏｌ／ＬＡＣｈ的作用较强，而１０－６和１０－５ｍｏｌ／ＬＡＣｈ无明显的抑制作用；②Ｍ型胆碱能受体激动剂毛果芸香碱（１０－８和１０－７ｍｏｌ／Ｌ）能明显减弱体外抗体生成，而Ｎ型受体激动剂烟碱（１０－８和１０－７ｍｏｌ／Ｌ）没有显著的减弱作用，Ｍ型受体拮抗剂阿托品（１０－７和１０－６ｍｏｌ／Ｌ）可完全阻断ＡＣｈ抑制体外抗体生成的作用；③ＡＣｈ分别在Ｂ细胞用ＳＲＢＣ刺激后３～４８ｈ中的６个不同时间与淋巴细胞作用，其抗体生成仍然是减少的。结论：ＡＣｈ可非浓度依赖性地抑制大鼠的体外抗体生成；此作用可能由Ｂ细胞上的Ｍ型胆碱能受体介导；且ＡＣｈ可能主要影响Ｂ细胞转化的后期过程。

EFFECT OF ACETYLCHOLINE ON THE ANTIBODY SYNTHESIS OF RATS IN VITRO

Aim and Methods: In the present study, the effect of acetylcholine (ACh) on the antibody synthesis and the primary mechanism of the action were investigated by means of the assay for antibody synthesis in vitro . The B lymphocytes in the mesenteric lymphaden of rats were stimulated with sheep red blood cells (SRBC) and incubated five days. Various concentrations of ACh (10 -10 to 10 -5 mol/L), muscarinic and nicotinic cholinergic receptor agonist and muscarinic receptor antagonist were respectively added to the lymphocyte suspension with SRBC. Results: ACh at 10 -10 to 10 -7 mol/L range significantly suppressed the antibody synthesis in vitro, having a stronger action at 10 -8 to 10 -7 mol/L, but having not remarked effect at 10 -6 to 10 -5 mol/L. Pilocarpine, a muscarinic cholinergic receptor agonist, significantly inhibited the antibody synthesis in vitro, but nicotine, a nicotinic cholinergic receptor agonist did not remarkably reduce the antibody synthesis in vitro. Atropine, a muscarinic receptor antagonist, abolished completely the inhibitory effect of ACh on the antibody synthesis in vitro. The antibody synthesis was still low when ACh was added at six different times to lymphocyte suspension that had been incubated with SRBC for 3 to 48 hours. Conclusion:ACh can cause concentration independent suppression of the antibody synthesis of rats in vitro, and the action of ACh may be mediated by the muscarinic receptor and occur in the later stage of B lymphocyte transformation.