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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。
In this experiment, we observed the effect of cholecystokinin (CCK-8) on the function of islet β cells damaged by interleukin-1β (IL-1β) on isolated islets of neonatal rats. And a preliminary analysis of its mechanism. The results showed that: (1) IL-1β (5,10,20U / ml) could inhibit the insulin secretion stimulated by glucose (20mmol / L). The inhibitory effect was dose-effect. The inhibition rates were 53.4% and 60% respectively. 5% and 70.7%. (2) CCK-8 has a protective effect on the function of islet β cells injured by IL-1. Prophylactic administration of CCK-8 (10 -10, 10 -9, 10 -8, 10 -7 mol / L) prevented IL-1β from stimulating glucose-stimulated insulin secretion Inhibition. Therapeutic administration of CCK-8 also restored the ability of the islets to glucose-stimulated insulin secretion. (3) CCK A receptor blocker L364718 (10nmol / L) can block the protective effect of CCK-8, indicating that this effect may be achieved through the CCK receptor. (4) While IL-1β inhibits insulin secretion, it can increase cGMP level in islet tissue, while CCK-8 can prevent IL-1-induced elevation of cGMP level.