右美沙芬可调节由海藻酸诱导的AP-1 DNA结合活性。

Dextromethorphan modulates the AP-1 DNA-binding activity induced by kainic acid.

作者信息

Kim H C, Bing G, Jhoo W K, Ko K H, Kim W K, Lee D C, Shin E J, Hong J S

机构信息

Section of Pharmacology and Toxicology, Department of Pharmacy, College of Pharmacy, Kangwon National University, Korea Institute of Drug Abuse, Chunchon 200-701, South

出版信息

Brain Res. 1999 Apr 3;824(1):125-32. doi: 10.1016/s0006-8993(99)01155-5.

DOI:10.1016/s0006-8993(99)01155-5

PMID:10095051

Abstract

We have recently reported that dextromethorphan attenuates the neurotoxicity induced by kainic acid in a dose-related fashion. Pretreatments with dextromethorphan (50 mg/kg, p.o. x2) significantly reduced the activator protein-1 DNA-binding activity and the Fos-related antigen-immunoreactive protein induced by kainic acid (10 mg/kg, i.p.) in the CA1, but not the CA3 or the dentate gyrus sector of the rat hippocampus. Paradoxically, dextromethorphan itself caused an elevated activator protein-1 DNA-binding activity and Fos-related antigen-immunoreactive protein in the CA1 region which lasted for at least 4 days. The results suggest that the CA1 area is the critical site for mediating the putative neuroprotective effect induced by dextromethorphan.

摘要

我们最近报道，右美沙芬能以剂量相关的方式减轻海藻酸诱导的神经毒性。用右美沙芬（50毫克/千克，口服，每日两次）预处理可显著降低由海藻酸（10毫克/千克，腹腔注射）诱导的大鼠海马CA1区的活化蛋白-1 DNA结合活性和Fos相关抗原免疫反应性蛋白，但对CA3区或齿状回无此作用。矛盾的是，右美沙芬本身会导致CA1区活化蛋白-1 DNA结合活性和Fos相关抗原免疫反应性蛋白升高，且这种升高持续至少4天。结果表明，CA1区是介导右美沙芬假定神经保护作用的关键部位。