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目的 研究垂体腺苷酸环化酶激活肽（ＰＡＣＡＰ） ３８与ＰＡＣＡＰ２７ 在ＰＣ１２ 细胞突起生长中的作用，并探讨介导其作用的受体和细胞内第二信使机制。方法 采用ＰＣ１２细胞分散培养法，观察接种７２ ｈ 时ＰＣ１２ 细胞突起生长阳性细胞的百分比。结果 当ＰＡＣＡＰ３８ 和ＰＡＣＡＰ２７ 的浓度为１ ×１０－ ７ ～１ ×１０－ １１ ｍｏｌ·Ｌ－１ 之间时，均能诱导ＰＣ１２细胞突起生长，其中以１×１０ －９ ｍｏｌ·Ｌ－ １ 的浓度作用最明显，量效曲线呈“钟”形。ＰＡＣＡＰ Ⅰ型受体拮抗剂ＰＡＣＡＰ６～３８和ｃＡＭＰ依赖的蛋白激酶抑制剂ＲｐｃＡＭＰＳ 能显著地抑制ＰＡＣＡＰ诱导ＰＣ１２ 细胞突起生长的作用，而蛋白激酶Ｃ 抑制剂Ｈ７ 却没有这个作用。结论 ＰＡＣＡＰ３８ 和ＰＡＣＡＰ２７均能诱导ＰＣ１２ 细胞突起生长，该作用是由ＰＡＣＡＰ Ⅰ型受体介导的，是通过细胞内ｃＡＭＰ 依赖的蛋白激酶系统实现的
Objective To investigate the role of pituitary adenylate cyclase-activating peptide (PACAP) 38 and PACAP27 in the process of prominence of PC12 cells and to explore the mechanism of the receptor and intracellular second messengers that mediate its role. Methods PC12 cells were cultured by dispersion method to observe the percentage of neurite outgrowth in PC12 cells at 72 h after inoculation. Results Proliferation of PC12 cells was induced when the concentration of PACAP38 and PACAP27 was between 1 × 10-7 ~ 1 × 10-11 mol·L-1, and the concentration of 1 × 10 -9 mol·L-1 The most obvious effect, the dose-response curve was “bell” shape. PACAP6 ~ 38, a kind of PACAP receptor antagonist, and RpcAMPS, a cAMP-dependent protein kinase inhibitor, significantly inhibited PACAP-induced PC12 cell proliferation, whereas protein kinase C inhibitor H7 did not. Conclusions Both PACAP38 and PACAP27 induce the proliferation of PC12 cells, which is mediated by PACAP type Ⅰ receptors and is mediated by the intracellular cAMP-dependent protein kinase system