孤啡肽/痛敏肽激活蛋白激酶C，且此效应是通过磷脂酶C/Ca2+途径介导的。

Nociceptin/orphanin FQ activates protein kinase C, and this effect is mediated through phospholipase C/Ca2+ pathway.

作者信息

Lou L G, Ma L, Pei G

机构信息

Shanghai Institute of Cell Biology, Chinese Academy of Sciences, China.

出版信息

Biochem Biophys Res Commun. 1997 Nov 17;240(2):304-8. doi: 10.1006/bbrc.1997.7654.

DOI:10.1006/bbrc.1997.7654

PMID:9388473

Abstract

The effect of nociceptin/orphanin FQ (N/OFQ) on protein kinase C (PKC) was investigated in Chinese hamster ovary cells stably expressing opioid receptor-like (ORL1) receptor (CHO-ORL1 cells). N/OFQ significantly activated PKC in CHO-ORL1 cells with EC50 of 0.2 nM. This response was blocked by PKC inhibitors chelerythrine and Gö 6976, and by pretreatment of cells with pertussis toxin (PTX). The inhibition of PKC activation by N/OFQ was also achieved by use of Ca(2+)-chelators and phospholipase C (PLC) inhibitor U-73122. These results indicate that N/OFQ can effectively activate PKC via ORL1 receptor, and suggest the activation involve the PLC/Ca2+ system.

摘要

在中国仓鼠卵巢细胞（CHO-ORL1细胞）中稳定表达阿片样受体（ORL1），研究了痛敏肽/孤啡肽FQ（N/OFQ）对蛋白激酶C（PKC）的影响。N/OFQ在CHO-ORL1细胞中显著激活PKC，其半数有效浓度（EC50）为0.2 nM。蛋白激酶C抑制剂白屈菜红碱和Gö 6976以及用百日咳毒素（PTX）预处理细胞可阻断此反应。使用钙螯合剂和磷脂酶C（PLC）抑制剂U-73122也可抑制N/OFQ对PKC的激活。这些结果表明，N/OFQ可通过ORL1受体有效激活PKC，并提示该激活涉及PLC/Ca2+系统。