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Activation of metabotropic glutamate receptor 5 reduces the secondary brain injury after traumatic brain injury in rats.

Abstract：

:A wealth of evidence has shown that microglia-associated neuro-inflammation is involved in the secondary brain injury contributed to the poor outcome after traumatic brain injury (TBI). In vitro studies were reported that activation of metabotropic glutamate receptor 5 (mGluR5) could inhibit the microglia-associated inflammation in response to lipopolysaccharide and our previous study indicated that mGluR5 was expressed in activated microglia following TBI. However, there is little known about whether mGluR5 activation can provide neuro-protection and reduce microglia-associated neuro-inflammation in rats after TBI. The goal of the present study was to investigate the effects of mGluR5 activation with selective agonist CHPG, on cerebral edema, neuronal degeneration, microglia activation and the releasing of pro-inflammatory cytokines, in a rat model of TBI. Rats were randomly distributed into various subgroups undergoing the sham surgery or TBI procedures, and 250 nmol of CHPG or equal volume vehicle was given through intracerebroventricular injection at 30 min post-TBI. All rats were sacrificed at 24 h after TBI for the further measurements. Our data indicated that post-TBI treatment with CHPG could significantly reduce the secondary brain injury characterized by the cerebral edema and neuronal degeneration, lead to the inhibition of microglia activation and decrease the expression of pro-inflammatory cytokines in both mRNA transcription and protein synthesis. These results provide the substantial evidence that activation of mGluR5 reduces the secondary brain injury after TBI, in part, through modulating microglia-associated neuro-inflammation.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Wang JW,Wang HD,Cong ZX,Zhang XS,Zhou XM,Zhang DD

doi

10.1016/j.bbrc.2012.12.046

subject

Has Abstract

pub_date

2013-01-18 00:00:00

pages

1016-21

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(12)02377-7

journal_volume

430

pub_type

杂志文章

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