摘要
本实验在分离培养的新生大鼠胰岛上,观察了胆囊收缩素(CCK-8)对白细胞介素-1β(IL—1β)损伤的胰岛β细胞功能的影响。并就其机制进行初步分析。结果表明:(1)IL—1β(5,10,20U/ml)能抑制葡萄糖(20mmol/L)刺激的胰岛素分泌,其抑制作用具有量效关系,抑制率分别为53.4%,60.5%和70.7%。(2)CCK-8对IL-1损伤的胰岛β细胞的功能具有保护作用。预防性地给予CCK-8(10 ̄(-10),10 ̄(-9),10 ̄(-8),10 ̄(-7)mol/L)能防止IL-1β对葡萄糖刺激的胰岛素分泌的抑制作用。治疗性地给予CCK-8也能恢复胰岛对葡萄糖刺激的胰岛素分泌的能力。(3)CCK A型受体阻断剂L364718(10nmol/L)能阻断CCK-8的保护作用,表明这一作用可能是通过CCK受体实现的。(4)IL-1β抑制胰岛素分泌的同时,能升高胰岛组织内cGMP水平,而CCK-8能阻止IL-1引起的cGMP水平的升高。
The purpose of the present study was to investigate the effects of cholecystokinin-octapeptide(CCK-8)on interleukin-1β(IL-1β)inhibited insulin secretion in cultured newbornislets and its mechanism. The results were as follows:(1) IL-1β(5、10、20U/ml)signiflcantlyinhibited glucose-stimulated insulin secretion in a dose-dependent manner,with the inhibitoryrate being 53.4%、60.5% and 70.7%, respectively.(2)Administration of CCK- 8(10 ̄(-10), 10 ̄(-9),10 ̄(-8) and 10 ̄(- 7)mol/ L) either before or after IL-1βcould abolish the inhibitory effect of IL-1β.(3)CCK A-type receptor antagonist L364718(10nmol/L) could block this protective effect ofCCK-8.(4)IL-1β(10U/ml) increased the level of cGMP in islets and CCK-8(10 ̄(-9)mol/L)could prevent IL-1β from increasing the level of cGMP. These results indicate that CCK-8 canprotect the function of islet cells against the injurious effect of IL-1β. This action of CCK-8 isprobably mediated by CCK receptor and may be related to the reduction of nitric oxide produc-tion.
出处
《中国应用生理学杂志》
CSCD
1995年第3期209-212,共4页
Chinese Journal of Applied Physiology