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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。神经鞘磷脂作为第二信使也参与此过程
Objective To observe the effect of pituitary adenylyl cyclase activating polypeptide (PACAP) on the growth of human pancreatic cancer cell lines and determine whether sphingomyelin participates in post-receptor signaling as a second messenger. Methods Human pancreatic cancer cell lines JF30 5, HS76 6T, ASPC 1 were cultured and passaged. Different concentrations of PACAP1 38 (10 -6 ~ 10 -12 mol / L) were added to the three kinds of cancer cells respectively. The cell proliferation was observed by MTT assay. Determination of Cellular Sphingomyelin by Thin Layer Chromatography. Radioimmunoassay was used to determine intracellular cAMP content. Fura 2 / AM determination of intracellular free Ca2 + concentration. Results PACAP1 38 promoted the growth of JF30 5, HS76 6T and ASPC 1 cells. PACAP1 38 increased the production of intracellular sphingomyelin, cAMP and Ca2 +. Somatostatin significantly inhibited the growth of JF30 5 cells induced by PACAP1 38. Conclusion PACAP1 3 8 promotes the proliferation of human pancreatic cancer cell lines. Post-PACAP signaling pathway: (1) adenylate cyclase pathway; (2) calmodulin pathway. Sphingomyelin is also involved in this process as a second messenger