Autor: |
Yi HA; Department of Neurology, Keimyung University School of Medicine, Keimyung University, Choong-Gu, Daegu, South Korea., Yi SD, Jang BC, Song DK, Shin DH, Mun KC, Kim SP, Suh SI, Bae JH |
Jazyk: |
angličtina |
Zdroj: |
Clinical and experimental pharmacology & physiology [Clin Exp Pharmacol Physiol] 2005 Dec; Vol. 32 (12), pp. 1097-103. |
DOI: |
10.1111/j.1440-1681.2005.04305.x |
Abstrakt: |
The aim of the present study was to investigate the effects of glucosamine on lipopolysaccharide (LPS)-induced cellular activation in microglia and to evaluate the inhibitory mechanisms involved. Lipopolysaccharide (100 ng/mL) was used for the activation of primary cultured rat microglial or BV2 microglial cells. Changes in intracellular Ca2+ levels and outward K+ currents were measured using fura-2/AM and whole-cell patch-clamp methods, respectively. Lipopolysaccharide-induced expression of tumour necrosis factor (TNF)-alpha mRNA was analysed by reverse transcription-polymerase chain reaction. Lipopolysaccharide transformed cell morphology into an amoeboid shape in vitro and induced microglial activation in vivo, as measured by immunohistochemical staining, but glucosamine inhibited this activation. Glucosamine also inhibited LPS-induced Ca2+ influx, outward K+ currents and TNF-alpha mRNA expression, which are typically representative of microglial activation. 4. The results suggest that the inhibitory mechanisms of glucosamine on LPS-induced microglial activation include inhibition of Ca2+ influx and outward K+ currents, as well as downregulation of the microglial activator gene TNF-alpha. |
Databáze: |
MEDLINE |
Externí odkaz: |
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