Chen W F, Chen L, Lu X W, Chen J J
Department of Physiology, The Medical College of Qingdao University, Qingdao 266021.
Sheng Li Xue Bao. 1999 Jun;51(3):253-7.
With the use of beta-EP microinjection into the central nervous system, spectrophotometrical analysis and immunochemical method we studied the effect of beta-Endorphin (beta-EP) on plasma sialic acid (SA) level. The results indicate: (1) The plasma SA level was significantly decreased after microinjection of beta-EP into the lateral ventricle (LV); (2) When beta-EP was microinjection into nucleus arcuatus (ARC), the plasma SA level was significantly decreased (P < 0.05). This effect can be blocked by i.v. atropine or vagotomy; (3) Microinjection of beta-EP into ARC can cause the increase of CD3, CD4 and CD4/CD8, while CD8 was decreased. The above results suggest that the possible mechanism underlying the decrease of plasma SA level is mediated by cholinergic muscarinic receptor, and the cellular immune function is enhanced.
通过向中枢神经系统微量注射β-内啡肽(β-EP)、分光光度分析及免疫化学方法,我们研究了β-内啡肽(β-EP)对血浆唾液酸(SA)水平的影响。结果表明:(1)向侧脑室(LV)微量注射β-EP后,血浆SA水平显著降低;(2)当向弓状核(ARC)微量注射β-EP时,血浆SA水平显著降低(P<0.05)。静脉注射阿托品或切断迷走神经可阻断此效应;(3)向ARC微量注射β-EP可使CD3、CD4及CD4/CD8升高,而CD8降低。上述结果提示,血浆SA水平降低的可能机制是由胆碱能毒蕈碱受体介导的,并且细胞免疫功能增强。