环磷酸腺苷（cAMP）增强β-淀粉样蛋白诱导的小胶质细胞一氧化氮释放。

cAMP potentiates beta-amyloid-induced nitric oxide release from microglia.

作者信息

Pyo H, Jou I, Jung S, Joe E

机构信息

Department of Pharmacology, Ajou University School of Medicine, Suwon, Kyunggi-do, Korea.

出版信息

Neuroreport. 1999 Jan 18;10(1):37-40. doi: 10.1097/00001756-199901180-00007.

DOI:10.1097/00001756-199901180-00007

PMID:10094129

Abstract

The beta-amyloid peptide (Abeta) has been known to activate microglia and to induce release of nitric oxide (NO). In this study, we examined the effect of cAMP on Abeta-induced microglial activation using cultured rat brain microglia. Dibutyryl-cAMP (dbcAMP) and 3-isobutyl-1-methylxanthine (IBMX) significantly potentiated Abeta(25-35)- or Abeta(1-42)-induced NO release in a dose-dependent manner. The increase in NO release was due to the increased expression of inducible nitric oxide synthase (iNOS). However, forskolin, an adenylate cyclase activator, weakly increased NO release at 10-50 microM but caused a decrease at 100 microM. These results suggest that increase in intracellular cAMP could potentiate microglial activation induced by Abeta.

摘要

已知β-淀粉样肽（Aβ）可激活小胶质细胞并诱导一氧化氮（NO）释放。在本研究中，我们使用培养的大鼠脑小胶质细胞研究了环磷酸腺苷（cAMP）对Aβ诱导的小胶质细胞激活的影响。二丁酰环磷腺苷（dbcAMP）和3-异丁基-1-甲基黄嘌呤（IBMX）以剂量依赖的方式显著增强了Aβ（25-35）或Aβ（1-42）诱导的NO释放。NO释放的增加是由于诱导型一氧化氮合酶（iNOS）表达增加所致。然而，腺苷酸环化酶激活剂福斯可林在10-50微摩尔时微弱增加NO释放，但在100微摩尔时导致释放减少。这些结果表明，细胞内cAMP的增加可增强Aβ诱导的小胶质细胞激活。