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Differential effects on glial activation by a direct versus an indirect thrombin inhibitor.

Abstract：

:Thrombin is a potent regulator of brain function in health and disease, modulating glial activation and brain inflammation. Thrombin inhibitors, several of which are in clinical use as anti-coagulants, can reduce thrombin-dependent neuroinflammation in pathological conditions. However, their effects in a healthy CNS are largely unknown. In adult healthy mice, we compared the effects of treatment by the direct thrombin inhibitor dabigatran etexilate (DE), to those of warfarin, which acts by preventing vitamin K recycling essential for coagulation. After 4weeks, warfarin increased both astrocyte GFAP and microglia Iba-1 staining throughout the CNS; whereas DE reduced expression of both markers. Warfarin, but not DE, reduced sulfatide levels; and warfarin showed longer lasting changes in cerebellar gene expression. DE also reduced glial activation in a mouse model of Alzheimer's disease, although no changes in amyloid plaque burden were observed. These results suggest that treatment with direct thrombin inhibitors may be preferable to those agents which reduce vitamin K levels and have the potential to increase glial activation.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Marangoni MN,Braun D,Situ A,Moyano AL,Kalinin S,Polak P,Givogri MI,Feinstein DL

doi

10.1016/j.jneuroim.2016.05.018

subject

Has Abstract

pub_date

2016-08-15 00:00:00

pages

159-68

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(16)30127-8

journal_volume

297

pub_type

杂志文章

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