Abstract:
:Hypothermia is an effective neuroprotective treatment for brain injury caused by intracerebral hemorrhage (ICH). It is reported to reduce brain edema and neuronal cell death. Thrombin, a coagulation protease released from blood clots, is critical in brain edema formation following ICH. Protease activated receptor‑1 (PAR‑1), matrix metalloproteinase‑9 (MMP‑9) and aquaporin 4 (AQP4) are edema‑associated mediators that have been implicated in ICH pathology. In the present study, thrombin was used to induce brain edema in adult male Sprague‑Dawley rats. Differences between a focal mild hypothermic group (33±0.5˚C) and a normothermic group (37˚C) were investigated. Following hypothermia, brain water content and blood‑brain barrier (BBB) disruption was assessed at 6, 24 and 48 h and subsequently at 3, 5 and 7 days. At the same time, the mRNA and protein expression of PAR‑1, MMP‑9 and AQP4 were also determined. It was identified that brain water content and BBB disruption increased at 6 h and reached a maximal level at 24 h in the normothermic group. The mRNA and protein expression levels of PAR‑1, MMP‑9 and AQP4 started to increase at 24 h and reached a maximal level at 48 h. Focal mild hypothermia tended to significantly reduce brain water content, BBB disruption and PAR‑1, MMP‑9 and AQP expression at 24 and 48 h. The present data suggest that focal mild hypothermia is an effective treatment for edema formation through moderation of the mRNA and protein expression of PAR‑1, MMP‑9 and AQP4.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Gao D,Ding F,Lei G,Luan G,Zhang S,Li K,Wang D,Zhang L,Dai Ddoi
10.3892/mmr.2014.3111subject
Has Abstractpub_date
2015-04-01 00:00:00pages
3009-14issue
4eissn
1791-2997issn
1791-3004journal_volume
11pub_type
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