PMID- 15692122
OWN - NLM
STAT- MEDLINE
DCOM- 20051006
LR  - 20220311
IS  - 1524-4628 (Electronic)
IS  - 0039-2499 (Linking)
VI  - 36
IP  - 3
DP  - 2005 Mar
TI  - Tuftsin fragment 1-3 is beneficial when delivered after the induction of 
      intracerebral hemorrhage.
PG  - 613-8
AB  - BACKGROUND AND PURPOSE: Microglial activation may contribute to the pathogenesis 
      of the brain injury in intracerebral hemorrhage (ICH). We have reported that the 
      tripeptide macrophage/microglial inhibitory factor (MIF), Thr-Lys-Pro, inhibits 
      microglial activation and results in functional improvement when given before the 
      onset of hemorrhage. In this study, we investigate the protection and efficacy of 
      treatment when MIF is administered 2 hours after collagenase injection. METHODS: 
      ICH was induced by injecting bacterial collagenase into the caudate nucleus; 100 
      microL MIF (500 micromol/L) was delivered via a micro-osmotic pump. Infusion of 
      MIF or saline (control) was initiated 2 hours after collagenase injection and 
      continued for 24 or 72 hours. Microglial activation and macrophage infiltration 
      were assessed by 5-d-4 and F4/80 immunofluorescence, respectively. Production of 
      reactive oxygen species was visualized by in situ detection of ethidium. 
      Degenerating neurons were assessed by Fluoro-Jade B staining. Neurological 
      deficits, brain injury volumes, and brain edema were assessed at 24 and 72 hours 
      after MIF/saline treatment. RESULTS: MIF can inhibit microglial activation and 
      macrophage infiltration, attenuate the numbers of ethidium-positive cells 
      compared with the saline-treated control mice, reduce the injury volume, edema, 
      and degenerating neurons, and improve the neurological functional outcome. 
      CONCLUSIONS: Activated microglia/macrophages are important contributors to brain 
      injury after ICH. MIF could be a valuable neuroprotective agent for the treatment 
      of ICH, if treatment is initiated soon after the onset of hemorrhage.
FAU - Wang, Jian
AU  - Wang J
AD  - Department of Pharmacological Sciences, University Medical Center at Stony Brook, 
      Stony Brook, NY 11794-8651, USA.
FAU - Tsirka, Stella E
AU  - Tsirka SE
LA  - eng
GR  - R01NS042168/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20050203
PL  - United States
TA  - Stroke
JT  - Stroke
JID - 0235266
RN  - 0 (Macrophage Migration-Inhibitory Factors)
RN  - 0 (Peptide Fragments)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 3.4.24.- (Collagenases)
RN  - QF5336J16C (Tuftsin)
SB  - IM
MH  - Animals
MH  - Brain Injuries/*prevention & control
MH  - Caudate Nucleus/pathology
MH  - Cell Death/drug effects
MH  - Cerebral Hemorrhage/*chemically induced/complications
MH  - Collagenases/adverse effects
MH  - Edema/metabolism
MH  - Macrophage Migration-Inhibitory Factors/metabolism/physiology/therapeutic use
MH  - Macrophages/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Microglia/physiology
MH  - Neurons/drug effects
MH  - Peptide Fragments/*therapeutic use
MH  - Psychomotor Disorders/etiology/prevention & control
MH  - Reactive Oxygen Species/metabolism
MH  - Stroke Volume/drug effects
MH  - Tuftsin/*therapeutic use
EDAT- 2005/02/05 09:00
MHDA- 2005/10/07 09:00
CRDT- 2005/02/05 09:00
PHST- 2005/02/05 09:00 [pubmed]
PHST- 2005/10/07 09:00 [medline]
PHST- 2005/02/05 09:00 [entrez]
AID - 01.STR.0000155729.12931.8f [pii]
AID - 10.1161/01.STR.0000155729.12931.8f [doi]
PST - ppublish
SO  - Stroke. 2005 Mar;36(3):613-8. doi: 10.1161/01.STR.0000155729.12931.8f. Epub 2005 
      Feb 3.