CCK-8对IL-1β诱导大鼠滑膜细胞株RSC-364增殖的影响

Effect of CCK-8 on IL-1β-induced RSC-364 proliferation

目的研究八肽胆囊收缩素(CCK-8)对IL-1β诱导大鼠滑膜细胞增殖的影响及相关机制。方法应用噻唑蓝(MTT)比色法检测CCK-8对IL-1β诱导RSC-364细胞增殖的影响;应用Westernblot检测CCK-8对IL-1β诱导RSC-364细胞p38MAPK磷酸化的影响。结果CCK-8剂量依赖性(10-12、10-10、10-8、10-6mol.L-1)抑制IL-1β诱导的RSC-364细胞增殖;CCK-8剂量依赖性(10-10、10-8、10-6mol.L-1)抑制了IL-1β诱导的RSC-364细胞p38MAPK的磷酸化;且CCK-8A、B受体拮抗剂CR1409或CR2945均减弱了CCK-8的抑制效应。结论CCK-8剂量依赖性抑制了IL-1β诱导的RSC-364细胞增殖,该作用由CCK-AR和CCK-BR介导,并可能通过抑制p38MAPK磷酸化而实现的。

Aim To investigate the effects and mechanisms of CCK-8 on IL-1β induced proliferation of RSC-364, a rat fibroblast-like synovial cell line. Methods MTT colorimetric assay and Western blot were used to measure cell proliferation and p38MAPK phosphorylation level to elucidate the mechanism of CCK-8 in IL-1β induced RSC-364 proliferation. Results CCK-8 significantly inhibited IL-1β-induced RSC-364 proliferation at 10^-12, 10^-10, 10^-8, 10^-6 mol·L^-1, and IL-1β-activated p38MAPK activity at 10^-10, 10^-8, 10^-6 mol·L^-1 in a dose-dependent manner. The effect of CCK-8 was blocked by CR1409 （a CCKA-receptor antagonist） and CR2945 （a CCKB-receptor antagonist）. Conclusion CCK-8 inhibits IL-1β-induced RSC-364 proliferation, probably by reducing p38MAPK activity through CCKA and CCKB receptors.