Figure 1.
Histological characteristics of cerebral cortex neurons in rats exposed to EMP radiation (n = 6).
A, The highlighted box is the observation region (scale bar = 50 µm). B–E, Representative HE staining of cerebral cortex neurons in control rats or rats at 1, 6 and 24 h after exposure to EMP radiation. Damaged neurons are characterized by a darkly stained nucleus and cytoplasm (arrow) (scale bar = 50 µm). F, The number of abnormal neurons in the cerebral cortex. The data are presented as the mean±SEM. ***P<0.01 vs. control group. G, Waveform of EMP. The EMP (peak-intensity 400 kV/m, rise-time 10 ns, pulse width 350 ns, 200 pulses) was generated by a spark gap pulse generator and transmitted into a Gigahertz transverse electromagnetic cell.
Figure 2.
Effect of sevoflurane on neuronal morphology and degeneration of the cerebral cortex in rats exposed to EMP radiation (n = 6).
A, Representative Nissl staining of cerebral cortex neurons in rats at 24 h after exposure to EMP radiation. The arrows indicate the morphology of abnormal neurons (scale bar = 50 µm). B, The density of normal neurons in the cerebral cortex at 24 h after EMP radiation. C, Representative FJC staining of cerebral cortex neurons in rats at 24 h after exposure to EMP radiation. Degenerative neurons were stained brightly by FJC. The arrows indicate the FJC-positive cells (scale bar = 50 µm). D, The number of FJC-positive neurons in the cerebral cortex at 24 h after EMP exposure. The data are presented as the mean±SEM. *P<0.05 vs. EMP group.
Figure 3.
Effect of sevoflurane on the ultrastructure of the cerebral cortex neurons of rats at 24 h after EMP (n = 6).
A, Electron microscopic image of normal cerebral cortex neurons. B and C, Electron microscopic image of cerebral cortex neurons at 24 h after EMP radiation. The shape of the neurons became obviously irregular. Mitochondria in the cytoplasm swelled to a spherical shape, the rough endoplasmic reticulum was cystic and the nuclear membrane was sunken, damaged and collapsed to varying degrees. D, Representative electron microscopic image of cerebral cortex neurons treated with 2% sevoflurane. Scale bar = 1 µm. * indicates: mitochondria in the cytoplasm; Triangular arrowheads indicates: endoplasmic reticulum; Arrow indicates nuclear membrane.
Figure 4.
Effect of sevoflurane on the neurobehavioral ability of rats exposed to EMP radiation (n = 12).
A and B, Motor function was assessed by a n open-field test at 24 h after EMP exposure. C and D, Learning and memory abilities were assessed by the Morris water maze and measured at 24 h after EMP exposure. *, P<0.05 and **, P<0.01.
Figure 5.
Effect of sevoflurane on cell viability, LDH release, MDA level and SOD activity of cerebral cortical neurons exposed to EMP radiation.
The cell viability (A), LDH release (B), MDA level (C) and SOD activity (D) were evaluated at 24 h after exposure to EMP radiation. The cell viability in the control group (normal cell group) was normalized to 100%. The values represent the mean (% of control) ± SEM of each group in this experiment. ##, P<0.01 and ####, P<0.001 vs. control group; *, P<0.05 and **, P<0.01 vs. EMP group.
Figure 6.
Effect of sevoflurane on apoptosis of cerebral cortical neurons exposed to EMP radiation.
A, Representative TUNEL staining of cerebral cortical neurons at 24 h after exposure to EMP radiation. The TUNEL-positive neurons are represented in green. Scale bar = 100 mm. B, The number of TUNEL-positive cells in each group. ###, P<0.001 vs. control group; *, P<0.05 vs. EMP group.
Figure 7.
Expression of active caspase-3, Bcl-2 and Bax in cerebral cortical neurons exposed to EMP radiation.
A, Representative western blot of active caspase-3 at 24 h after exposure to EMP radiation. B, Quantification of relative changes in active caspase-3 expression. C, Representative western blotting of Bcl-2 and Bax at 24 h after exposure to EMP radiation. D and E, Quantification of relative changes in Bcl-2 and Bax expression. The data are normalized to β-actin. ##, P<0.05 vs. control group; *, P<0.05 vs. EMP group.