CCKB受体激活导致大鼠胶质瘤C6细胞中[3H]胸苷掺入增加。

CCKB receptor activation results in increased [3H]thymidine incorporation in rat glioma C6 cells.

作者信息

Kaufmann R, Henklein P, Nowak G

机构信息

Max-Planck-Gesellschaft, Research Unit Pharmacological Hemostaseology at the Friedrich Schiller University, Jena, Germany.

出版信息

Neuropeptides. 1995 Nov;29(5):241-4. doi: 10.1016/0143-4179(95)90031-4.

DOI:10.1016/0143-4179(95)90031-4

PMID:8587658

Abstract

Cholecystokinin (CCK) is known to stimulate cell proliferation but involvement of CCKB type receptors has not been exactly demonstrated so far. We examined the effect of CCK-8S and two receptor agonists on rat glioma C6 cells when using different CCKB receptor agonists and antagonists. Both CCK-8S and CCKB receptor agonists BC 264 and Suc-Trp-N(Me)Nle-Asp-Phe-NH2 stimulate [3H]thymidine incorporation. These effects were inhibited by CCKB receptor antagonist L-365,260 over 100-fold more effectively than it was seen by using CCKA receptor antagonist L-364,718. The data indicate that CCKB receptor agonists are potent stimulants of rat glioma C6 cell DNA synthesis suggesting that CCKB receptor activation is involved in cell proliferation within the central nervous system.

摘要

已知胆囊收缩素（CCK）可刺激细胞增殖，但迄今为止，CCK B型受体的参与作用尚未得到确切证实。我们在使用不同的CCK B受体激动剂和拮抗剂时，研究了CCK-8S和两种受体激动剂对大鼠胶质瘤C6细胞的影响。CCK-8S和CCK B受体激动剂BC 264以及Suc-Trp-N（Me）Nle-Asp-Phe-NH2均可刺激[3H]胸腺嘧啶核苷掺入。CCK B受体拮抗剂L-365,260对这些作用的抑制效果比CCK A受体拮抗剂L-364,718高出100多倍。数据表明，CCK B受体激动剂是大鼠胶质瘤C6细胞DNA合成的强效刺激剂，提示CCK B受体激活参与中枢神经系统内的细胞增殖。