摘要
目的 观察垂体腺苷酸环化酶激活多肽 (pituitaryadenylatecyclaseactivatingpolypeptide,PACAP)对人胰腺癌细胞株的生长调控作用 ;并确定神经鞘磷脂是否作为第二信使参与受体后信息传导。方法 人胰腺癌细胞株JF30 5 ,HS76 6T ,ASPC 1进行细胞培养 ,传代。分别加入不同浓度的PACAP1 38(10 -6～ 10 -12 mol/L)于三种癌细胞中。应用MTT法观察细胞增殖程度。薄层层析法测定细胞神经鞘磷脂。放射免疫法测定细胞内cAMP含量。Fura 2 /AM测定细胞内游离Ca2 +浓度。结果PACAP1 38促进JF30 5 ,HS76 6T ,ASPC 1细胞的生长 ;PACAP1 38增加细胞内神经鞘磷脂、cAMP、Ca2 +的生成 ;生长抑素可明显抑制PACAP1 38诱导的JF30 5细胞的生长等作用。结论 PACAP1 3 8促进人胰腺癌细胞株的增殖。PACAP受体后信息传递途径 :(1)腺苷酸环化酶途径 ;(2 )钙 钙调素途径。
Objective To investigate the role pituitary adenylate cyclase activating polypeptide (PACAP) in the growth modulation of PACAP of human pancreas carcinoma cells and determine whether sphingomyolin (SM) may act as a second messenger involved in the postreceptor signal transduction. Methods Human pancreas carcinoma cell strains, JF305, HS766T and ASPC 1 cells were cultivated, reproduced and then treated with PACAP 1 38 (10 -12 -10 -6 M). The amounts of proliferated carcinoma cells were estiimated with Mosmann's method (MTT). The concentrations of intracellular SM in cells were determined with thin layer chromotograph. Intracellular adenosine monophosphate and Ca 2+ levels were detected by radioimmunoassay and Fura 2/AM respectively. Results It was found that three kind of human pancreatic cancer cells were proliferated and the intracellular levels of SM, cAMP and cytosolic Ca 2+ were increased by treating PACAP 1 38 . The effect of PACAP 1 38 in JF305, HS766T and ASPC 1 could be inhibited by Somatostatin. Conclusion PACAP 1 38 may play a role in the proliferation of human pancreatic cancer cells. The postreceptorsignal transduction of PACAP may be mediated by both adenosine cyclinase and Calcium calmodin pathways. SM may be a second messenger involved in this process.
出处
《中华消化杂志》
CAS
CSCD
北大核心
2001年第2期86-89,共4页
Chinese Journal of Digestion
关键词
垂体腺苷酸环化酶激活多肽
神经鞘磷脂
人胰腺癌细胞株
胰腺癌
Pituitaty adenylate cyclase activating polyopeptide
Sphingomyolin
Human pancreatic cancer cell strains
