Figure 8. Effects of FFA on the TRPM4 channel in the
neurovascular unit after cardiac arrest and cardiopulmonary
resuscitation.
qPCR results of Trpm4 in the brain of the sham, vehicle and FFA
groups at 24 h after return of spontaneous circulation. (B )
Western blot analysis of TRPM4 in the brain of the sham group, vehicle
and FFA groups at 24 h after return of spontaneous circulation and
quantitative graph. (C ) Representative photomicrographs of
immunofluorescence staining for TRPM4 (green) and several cell markers
(red) including, NeuN, Iba1, GFAP and CD31 in the brain at 24 h after
return of spontaneous circulation. Scale bar, 50 μm.
*P <0.05, **P <0.01 versus the sham
group; #P <0.05 versus the vehicle group. FFA:
flufenamic acid; GFAP: glial fibrillary acidic protein; Iba1: ionized
calcium-binding adapter molecule 1; NeuN: neuronal nucle.Figure 9. Effects of FFA on neurologic outcome and
histological injury in Trpm4−/− mice after
cardiac arrest and cardiopulmonary resuscitation.
(A ) Results of agarose gel electrophoresis of tail DNA from WT
and KO mice. (B ) Neurological function score of survived mice
from WT, KO and KO (FFA) groups at 3 days and 7 days after return of
spontaneous circulation. (C ) Representative photomicrographs of
post-cardiac arrest neuropathological damages characterized by
immunofluorescence staining for NeuN, MAP2, GFAP, Iba1 in the
hippocampal CA1 region from each group at 7 days after return of
spontaneous circulation. Scale bar, 100 μm or 50 μm. (D )
Semi-quantitative results of NeuN, MAP2, Iba1, and GFAP.
**P <0.01, ***P <0.001 versus the WT
group. GFAP: glial fibrillary acidic protein; Iba1: ionized
calcium-binding adapter molecule 1; KO: vehicle-treatedTrpm4−/− mice; KO (FFA): flufenamic
acid-treated Trpm4−/− mice; MAP2:
microtubule-associated protein 2; NeuN: neuronal nucle; WT:
vehicle-treated wild-type mice.