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PubMed2002

Spatial and temporal profile of apoptosis following lateral fluid percussion brain injury.

OBJECTIVE: To investigate the spatial and temporal profile of neural cell apoptosis following traumatic brain injury (TBI). METHODS: In addition to morphological evidence of apoptosis, TUNEL histochemistry assay was used to identify DNA fragmentation in situ at both light and electron microscopic levels, whereas characteristic internucleosomal DNA fragmentation of apoptosis was demonstrated by DNA gel electrophoresis. RESULTS: Using TUNEL method, we detected massive cells with extensive DNA fragmentation in different regions of the brains of rats subjected to experimental traumatic brain injury. Compared with the sham controls, in the injured cortex, the apoptotic cells were detectable for up to 24 h and reached a peak at 1 week after injury. The number of apoptotic cells in the white matter h ad a significant increase as early as 12 h after injury and peaked at 1 wee k. The number of apoptotic cells increased in the hippocampus at 72 h, whereas i n the thalamus, the peak of apoptotic cells was at 2 weeks after injury. The number of apoptotic cells in most regions returned to sham values 2 months after in jury. Gel electrophoresis of DNA extracted from affected areas of the injured br ain revealed only internucleosomal fragmentation at 185-bp intervals, a feature originally described in apoptotic cell death. And no DNA ladder was detectable in the cortex and hippocampus contralateral to the injured hemisphere. CONCLUSIONS: These data suggest that in addition to the well described necrotic cell death, a temporal course of apoptotic cell death is initiated after brain trauma in selected brain regions.

Analysis of Variance↗
PubMed1999

Alterations of bcl-2, bcl-x and bax protein expressions in area CA-3 of rat hippocampus following fluid percussion brain injury.

OBJECTIVE: To investigate the alterations of bcl-2 gene family in the area of CA-3 in rats and the molecular mechanism of neuronal apoptosis following traumatic brain injury. METHODS: To investigate the alterations of bcl-2 gene family in the area of CA-3 in rats and the molecular mechanism of neuronal apoptosis following traumatic brain injury. RESULTS: The immunoreactivity of bcl-2 and bcl-x proteins decreased in the hippocampus ipsilateral impact site at 6 hours after injury, and this was the main cause of down-regulation of the value of (bcl-2+bcl-x)/ bax. During the period of 1-3 days after injury, bax protein expression increased significantly, while bcl-2 and bcl-x protein expressions decreased relatively slowly. The decreased value of (bcl-2+bcl-x)/ bax was mainly due to the bax up-regulation. CONCLUSIONS: The bcl-2 gene family is involved in neuronal apoptosis after traumatic brain injury, and the protein-expression alterations of the bcl-2 gene family members lead to apoptosis of the neuronal cells.

Journal Article↗
PubMed2001

[The development of a device producing brain injury by gas percussion].

The device is developed based on aerodynamical principle, measuring technique for feeble signal, and mechano-electronic integration. The left parietals of rats were made cranioectomy and injured by different pressure of gas source with the device and then the survival states, pathological changes and neurobehavioral changes of rats were observed.

Animals↗