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Results: 5

1.
Fig. 3.

Fig. 3. From: Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein.

Short-term application of ROS scavengers counteracts the cerebrovascular dysfunction in 12- to 15-month-old Tg2576 mice. Cerebrovascular responses are rescued by a 30-min neocortical application of MnTBAP (A–C) or gp91ds-tat (gp91ds) (E–G) but not by a scrambled peptide (sgp91) (E–G). Responses to adenosine are not attenuated in Tg2576 mice (D and H). *, P < 0.05 from vehicle; analysis of variance and Tukey's test; n = 5 per group. V, vehicle.

Laibaik Park, et al. Proc Natl Acad Sci U S A. 2008 January 29;105(4):1347-1352.
2.
Fig. 1.

Fig. 1. From: Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein.

Nox2 inactivation rescues the cerebrovascular dysfunction in Tg2576 mice. CBF responses to whisker stimulation (A) and topical neocortical application of acetylcholine (10 μM) (B), bradykinin (50 μM) (C), or adenosine (400 μM) (D) in young and aged WT, Nox2−/−, Tg2576, or Tg2576/Nox2−/− mice. *, P < 0.05 from young WT; #, P < 0.05 from young Tg2576; analysis of variance and Tukey's test; n = 5 per group.

Laibaik Park, et al. Proc Natl Acad Sci U S A. 2008 January 29;105(4):1347-1352.
3.
Fig. 4.

Fig. 4. From: Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein.

Brain Aβ and amyloid burden are not reduced in 12- to 15-month-old Tg2576 mice lacking Nox2. (A and B) SDS-soluble (A) and -insoluble (B) Aβ are not different in Tg2576 and Tg2576/Nox2−/− mice (P > 0.05; analysis of variance and Tukey's test; n = 12 per group). (C and D) The amyloid load is comparable between Tg2576 (C) and Tg2576/Nox2−/− mice (D). (E and F) The number of plaques (E) and plaque load (F) do not differ between Tg2576 and Tg2576/Nox2−/− mice (P > 0.05; n = 6 per group).

Laibaik Park, et al. Proc Natl Acad Sci U S A. 2008 January 29;105(4):1347-1352.
4.
Fig. 5.

Fig. 5. From: Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein.

Nox2 inactivation rescues the behavioral deficits in Tg2576 mice tested in a Y maze. The reduction in novel arm entry (A), time spent in the novel arm (B), and the increase in total arm visits (C) and defecation (D) observed in Tg2576 mice are not seen in Tg2576/Nox2−/− mice. *, P < 0.05, χ2 test in A and analysis of variance and the Newman–Keul test in B–D; n = 10–15 per group.

Laibaik Park, et al. Proc Natl Acad Sci U S A. 2008 January 29;105(4):1347-1352.
5.
Fig. 2.

Fig. 2. From: Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein.

Nox2 inactivation attenuates neuronal and vascular oxidative stress in 12–15-month-old Tg2576 mice. (A) Wild-type mice. Neurons immunolabeled with NeuN (a) are colocalized with the ROS (HE) signal (b), as shown by the merged image (c). Endothelial cells immunolabeled with CD31 (d) are also colocalized with the ROS signal (e and f). (Scale bar: 50 μm.) (B) Tg2576 mice. NeuN-positive neurons (a) are colocalized with the ROS signal (b and c). CD31-positive endothelial cells (d) are also colocalized with the ROS signal (e and f). (Scale bar: 50 μm.) (C) The increased ROS signal in Tg2576 is attenuated by the ROS scavenger MnTBAP and a NADPH peptide inhibitor (gp91-ds) but not by a scrambled peptide (sgp91ds) or in Tg2576/Nox2−/− crosses. *, P < 0.05 from WT; analysis of variance and Tukey's test; n = 5 per group.

Laibaik Park, et al. Proc Natl Acad Sci U S A. 2008 January 29;105(4):1347-1352.

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