Establishment of a mechanical injury model of rat hippocampal neurons in vitro / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To establish a simple, reproducible, and practical mechanical injury model of hippocampal neurons of Sprague-Dawley rats in vitro.</p><p><b>METHODS</b>Hippocampal neurons isolated from 1-2-day old rats were cultured in vitro. Mild, moderate and severe mechanical injuries were delivered to the neurons by syringe needle tearing, respectively. The control neurons were treated identically with the exception of trauma. Cell damage was assessed by measuring the Propidium Iodide (PI) uptaking at different time points (0.5, 1, 6, 12 and 24 hours) after injury. The concentration of neuron specific enolase was also measured at some time points.</p><p><b>RESULTS</b>Pathological examination showed that degeneration, degradation and necrosis occurred in the injured cultured neurons. Compared with the control group, the ratio of PI-positive cells in the injured groups increased significantly after 30 minutes of injury (P<0.05). More severe the damage was, more PI-positive neurons were detected. Compared with the control group, the concentration of neuron specific enolase in the injured culture increased significantly after 1 hour of injury (P<0.05).</p><p><b>CONCLUSIONS</b>The established model of hippocampal neuron injury in vitro can be repeated easily and can simulate the damage mechanism of traumatic brain injury, which can be used in the future research of traumatic brain injury.</p>

Correlation of cell apoptosis with brain edema and elevated intracranial pressure in traumatic brain injury / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To study the correlation between brain edema, elevated intracranial pressure (ICP) and cell apoptosis in traumatic brain injury (TBI).</p><p><b>METHODS</b>In this study, totally 42 rabbits in 7 groups were studied. Six of the animals were identified as a control group, and the remaining 36 animals were equally divided into 6 TBI groups. TBI models were produced by the modified method of Feeney. After the impact, ICP of each subject was recorded continuously by an ICP monitor until the animal was sacrificed at scheduled time. The apoptotic brain cells were detected by an terminal deoxynucleotide-transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. Cerebral water content (CWC) was measured with a drying method and calculated according to the Elliott formula. Then, an analysis was conducted to determine the correlation between the count of apoptotic cells and the clinical pathological changes of the brain.</p><p><b>RESULTS</b>Apoptotic cell count began to increase 2 h after the impact, and reached its maximum about 3 days after the impact. The peak value of CWC and ICP appeared 1 day and 3 days after the impact, respectively. Apoptotic cell count had a positive correlation with CWC and ICP.</p><p><b>CONCLUSIONS</b>In TBI, occurrence of brain edema and ICP increase might lead to apoptosis of brain cells. Any therapy which can relieve brain edema and/or decrease ICP would be able to reduce neuron apoptosis, thereby to attenuate the secondary brain damage.</p>

Effect of handportable mobiletelephone microwave radiation on rat central neuron apoptosis / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effect of handportable mobiletelephone microwave radiation on rat central nervous system by setting up rat model.</p><p><b>METHODS</b>80 healthy male SD rats (weighed about 200 g) were divided into 4 groups at random: control, radiation, decranium, decranium + radiation. TUNEL method was adopted used to detect the apoptosis of neurons after irradiation, then immunohistochemistry was used to detect Bcl-2, Bax expression in all brain tissue.</p><p><b>RESULTS</b>TUNEL positive rate, Bax and Bcl-2 positive cell numbers could be found in decranium + radiation group [(26.45 +/- 9.27)%, (23.5 +/- 3.58), (11.1 +/- 2.55) respectively]. There were significant differences among control [(9.59 +/- 2.55)%, 14.2 +/- 2.46, 7.0 +/- 1.14 respectively], decranium group [(9.52 +/- 1.93)%, 15.5 +/- 1.77, 7.4 +/- 1.76], radiation group [(10.04 +/- 3.62)%, 15.9 +/- 2.02, 7.2 +/- 1.07] (P < 0.01). But the difference was not found in the ratio of Bax to Bcl-2.</p><p><b>CONCLUSION</b>Microwave radiation did not affect the intact rat, but did promote the occurrence of neuron apoptosis in cranial defect rat. Bax, Bcl-2 gene participated in regulation of apoptosis. The intact cranium may be an important factor to protect the neurons against handportable mobiletelephone microwave radiation to some extent.</p>