AHPN reduces ischemic neuronal apoptosis and
preserves dendritic/synaptic integrity
in vitro. (a) Representative images of
TUNEL+ (in green) and
β-tubulin+ (in red) neurons and
quantitative analysis. Nuclei are counterstained with DAPI (blue).
Scale bars: 100 µm. Data are
means ± standard error.
*p ≤ 0.05,
compared with OGD and OGD/ROG controls, respectively.
+++p ≤ 0.001,
++p ≤ 0.01,
compared with non-hypoxic CTRL neurons;
**p ≤ 0.01,
*p ≤ 0.05,
compared with OGD or OGD/ROG controls. (b) Representative
microphotographs of primary cortical neurons dendrites stained for
MAP2 (green) and corresponding quantification. Nuclei are
counterstained with DAPI (blue). Scale bars: 100 µm.
Note the dose-dependent increase of MAP2 expression induced by AHPN
in both OGD and OGD/ROG treated neurons.
++p ≤ 0.01
compared with non-hypoxic CTRL neurons;
*p ≤ 0.05, compared
with OGD or OGD/ROG controls. (c,d) Representative reconstructions
and microphotographs of OGD (c) and OGD/ROG (d) primary cortical
neurons treated with AHPN. Dendrites are stained with MAP2 (green),
while spines are stained with PSD95 (red). Nuclei are counterstained
with DAPI (blue). Scale bars: 10 µm. Sholl analysis
of dendritic length with nested concentric spheres centred at the
cell soma and with a gradually increasing radius
(5 µm) showing cumulative dendritic length in the
function of cell soma distance, the integrated total dendritic
length, and the spine density of primary cortical neurons.
+p ≤ 0.05,
compared with non-hypoxic CTRL neurons,
**p ≤ 0.01,
*p ≤ 0.05,
compared with OGD or OGD/ROG controls.