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.