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Results: 8

1.
Figure 6

Figure 6. From: Attenuation of neonatal ischemic brain damage using a 20-HETE synthesis inhibitor.

(A) Double immunofluorescent staining of normal pig striatum shows co-localization of CYP4A with NeuN. (B) Double immunofluorescent staining on piglet putamen at 3 h of recovery from H-I shows co-localization of JNK1,2,3, p38 MAPK, and Erk1/2 with NeuN. Scale bar = 20 μm.

Zeng-Jin Yang, et al. J Neurochem. ;121(1):168-179.
2.
Figure 2

Figure 2. From: Attenuation of neonatal ischemic brain damage using a 20-HETE synthesis inhibitor.

Laser-Doppler flow (LDF) over somatosensory cortex (A) and microsphere-determined blood flow in putamen (B) during baseline, hypoxia, asphyxia, and first 6 h of recovery after H-I or equivalent time in sham-operated piglets (means ± SD; n = 4 per group). Piglets were treated with vehicle or 10 mg/kg of HET0016 at 5 min of recovery.

Zeng-Jin Yang, et al. J Neurochem. ;121(1):168-179.
3.
Figure 8

Figure 8. From: Attenuation of neonatal ischemic brain damage using a 20-HETE synthesis inhibitor.

Effect of 1 mg/kg of HET0016 treatment at 5 min of recovery on H-I–induced nitrative and oxidative stress in putamen at 3 h of recovery. Western blot analysis showed that HET0016 decreased H-I–induced 3-nitrotyrosine (A) and carbonyl (B) immunoreactivity on multiple protein bands in putamen of H-I piglets. Optical density (O.D.; means ± SD) was integrated over multiple protein bands for nitrotyrosine (14–191 kDa) and carbonyls (29–98 kDa). *P < 0.05 versus sham+vehicle group; #P < 0.05 versus H-I+vehicle group; one-way ANOVA followed by the Student-Newman-Keuls test.

Zeng-Jin Yang, et al. J Neurochem. ;121(1):168-179.
4.
Figure 4

Figure 4. From: Attenuation of neonatal ischemic brain damage using a 20-HETE synthesis inhibitor.

Western blot analysis showing effects of 1 mg/kg of HET0016 treatment at 5 min of recovery on phosphorylated Ser896 and Ser897 and total protein levels of NR1 in a membrane-enriched fraction of putamen at 3 h of recovery (n = 4 to 6 per group). Synaptophysin (Syn) was used as a loading control. Optical density (O.D.) data (means ± SD) were normalized to the sham+vehicle value. *P < 0.05 versus sham+vehicle group; # P < 0.05 versus H-I+vehicle group; one-way ANOVA followed by the Student-Newman-Keuls test.

Zeng-Jin Yang, et al. J Neurochem. ;121(1):168-179.
5.
Figure 7

Figure 7. From: Attenuation of neonatal ischemic brain damage using a 20-HETE synthesis inhibitor.

Western blot analysis showing effects of 1 mg/kg of HET0016 treatment at 5 min of recovery on levels of phosphorylated and total JNK1,2,3 (JNK), p38 MAPK (p38), and Erk1/2 in cytosol-enriched fraction of putamen from H-I piglets at 3 h of recovery or equivalent time in sham-operated piglets (n = 4 to 6 per group). β-actin (actin) was used as a loading control. Optical density (O.D.) data (means ± SD) were normalized to the sham+vehicle value; *P < 0.05 versus sham+vehicle group. # P < 0.05 versus H-I+vehicle group; one-way ANOVA followed by the Student-Newman-Keuls test.

Zeng-Jin Yang, et al. J Neurochem. ;121(1):168-179.
6.
Figure 3

Figure 3. From: Attenuation of neonatal ischemic brain damage using a 20-HETE synthesis inhibitor.

Western blot analysis showing effects of 1 mg/kg of HET0016 treatment at 5 min of recovery on phosphorylated Ser23 and Ser943 and total protein levels of Na+,K+-ATPase (NKA) in a membrane-enriched fraction of putamen at 3 h of recovery (n = 4 to 6 per group). Synaptophysin (Syn) was used as a loading control. NKA activity was measured in contralateral putamen. Optical density (O.D.) data (means ± SD) were normalized to the sham+vehicle value. *P < 0.05 versus sham+vehicle group; # P < 0.05 versus H-I+vehicle group; one-way ANOVA followed by the Student-Newman-Keuls test.

Zeng-Jin Yang, et al. J Neurochem. ;121(1):168-179.
7.
Figure 5

Figure 5. From: Attenuation of neonatal ischemic brain damage using a 20-HETE synthesis inhibitor.

Western blot analysis showing effects of microdialysis perfusion of 30 μM of 20-HETE in piglet putamen on phosphorylated and total protein levels of Na+,K+-ATPase (A) and NMDA receptor NR1 subunit (B) in a membrane-enriched fraction of putamen of piglets without H-I (n = 3 to 4 per group). Synaptophysin (Syn) was used as a loading control. Optical density (O.D.) data (means ± SD) were normalized to the value of vehicle-treated group. *P < 0.05 versus vehicle group, Student’s t-test. c: putamen contralateral to microdialysis probe; i: putamen ipsilateral to microdialysis probe; Veh: vehicle treatment.

Zeng-Jin Yang, et al. J Neurochem. ;121(1):168-179.
8.
Figure 1

Figure 1. From: Attenuation of neonatal ischemic brain damage using a 20-HETE synthesis inhibitor.

Effects of HET0016 on neuronal damage and neurologic deficits in piglets subjected to H-I. Piglets exposed to H-I or sham operation received vehicle, low-dose HET0016 (HET0016-L, 1 mg/kg), and high-dose HET0016 (HET0016-H, 10 mg/kg) treatment at 5 min of recovery. (A) Representative photographs of H&E-stained sections at 4 days of recovery show normal neuronal morphology (arrow head) and cytoarchitecture in putamen of sham-operated animals treated with vehicle. All H-I groups contained putaminal neurons that exhibited ischemic morphology (cytoplasmic microvacuolation, eosinophilia, and nuclear pyknosis, arrow) or that had lost distinct structure. However H-I piglets treated with low or high dose of HET0016 showed many neurons with normal morphology. Scale bar = 40 μm. (B) Quantitative results for viable putamen neurons (expressed as a percentage of the mean value of the sham+vehicle group). Data are means ± SD (n = 7 to 8 per group). *P < 0.05 versus sham-operated group; # P < 0.05 versus H-I vehicle group; ANOVA followed by the Student-Newman-Keuls test. (C) Neurologic scores during the 4-day recovery. Two-way ANOVA with repeated measured indicated a significant overall effect of treatment (P < .001) and recovery time (P < 0.001).

Zeng-Jin Yang, et al. J Neurochem. ;121(1):168-179.

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