Moody Terry W, Jensen Robert T, Fridkin Mati, Gozes Illana
National Cancer Institute, Medicine Branch, Rockville, MD 20850, USA.
J Mol Neurosci. 2002 Feb-Apr;18(1-2):29-35. doi: 10.1385/JMN:18:1-2:29.
The effects of a (N-stearyl, Norleucine17) vasoactive intestinal peptide hybrid ((SN)VIPhybrid) on cells stably transfected with VPAC,, VPAC2, or PAC1 receptors were investigated. (SN)VIPhybrid inhibited specific 125I-VIP binding to membranes derived from CHO cells transfected with VPAC, or VPAC2 receptors with high affinity (IC50 = 30 and 50 nM). (SN)VIPhyb inhibited specific 125I-PACAP-27 binding to membranes derived from NIH/3T3 cells transfected with PAC1 receptors with high affinity (IC50 = 65 nM). PACAP-27 caused cAMP elevation in NIH/3T3 cells transfected with PAC1 receptors and the increase cAMP caused by pituitary adenylated cyclase (PACAP) was inhibited by (SN)VIPhyb. Also, the increase in cAMP caused by VIP using CHO cells transfected with VPAC1 or VPAC2 receptors was antagonized by (SN)VIPhyb. These results indicate that (SN)VIPhyb is an antagonist for VPAC1, VPAC2, and PAC1 receptors.
研究了一种（N-硬脂酰基，去甲亮氨酸17）血管活性肠肽杂交体（（SN）VIP杂交体）对稳定转染VPAC1、VPAC2或PAC1受体的细胞的影响。（SN）VIP杂交体以高亲和力抑制125I-VIP与源自转染VPAC1或VPAC2受体的CHO细胞膜的特异性结合（IC50 = 30和50 nM）。（SN）VIP杂交体以高亲和力抑制125I-PACAP-27与源自转染PAC1受体的NIH/3T3细胞膜的特异性结合（IC50 = 65 nM）。PACAP-27在转染PAC1受体的NIH/3T3细胞中引起cAMP升高，垂体腺苷酸环化酶激活肽（PACAP）引起的cAMP增加被（SN）VIP杂交体抑制。此外，使用转染VPAC1或VPAC2受体的CHO细胞，VIP引起的cAMP增加被（SN）VIP杂交体拮抗。这些结果表明（SN）VIP杂交体是VPAC1、VPAC2和PAC1受体的拮抗剂。
