Hunan yi ke da xue xue bao = Hunan yike daxue xuebao = Bulletin of Hunan Medical University · 1999
[The phasic and regional variations of lipid peroxidation after diffuse brain injury in rats].
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Wang J
Аннотация
OBJECTIVE: Using a diffuse brain injury animal model, we studied the time course of lipid peroxidation in different regions of injured rat brains.
METHODS: 53 male SD rats were randomly divided into sham, post-traumatic 1, 2, 4, 7, 24 h groups (n = 8) to measure the MDA (malondialdehyde) at the bilateral frontal, temporal, parietal, striatum and brain stem, another 5 rats were researched for histological study.
RESULTS: At the frontal, parietal and brain stem, the MDA levels were 36.7%, 41.8% and 35.1%, respectively, higher than sham at one hour after injury (P < 0.01). The MDA levels in these regions continued to increase and peaked at 4 hours after the injury. The levels decreased slowly, and by 24 hours, they were still significantly higher than the sham control's. The elevation of MDA levels was less in the striatum and the temporal compared with above regions at one hour. Their rising rates were 16.9% and 13.3%, respectively(P < 0.01). The MDA levels in there two regions continued to increase even after 4 hours of injury, but the degree of elevation never exceeded 35%.
CONCLUSION: There is an immediate, post-traumatic burst of MDA production, suggesting the formation of free radicals after diffuse head injury. Even though all the regions sampled show the same effect, certain regions are less affected in this diffuse brain injury animal model.
METHODS: 53 male SD rats were randomly divided into sham, post-traumatic 1, 2, 4, 7, 24 h groups (n = 8) to measure the MDA (malondialdehyde) at the bilateral frontal, temporal, parietal, striatum and brain stem, another 5 rats were researched for histological study.
RESULTS: At the frontal, parietal and brain stem, the MDA levels were 36.7%, 41.8% and 35.1%, respectively, higher than sham at one hour after injury (P < 0.01). The MDA levels in these regions continued to increase and peaked at 4 hours after the injury. The levels decreased slowly, and by 24 hours, they were still significantly higher than the sham control's. The elevation of MDA levels was less in the striatum and the temporal compared with above regions at one hour. Their rising rates were 16.9% and 13.3%, respectively(P < 0.01). The MDA levels in there two regions continued to increase even after 4 hours of injury, but the degree of elevation never exceeded 35%.
CONCLUSION: There is an immediate, post-traumatic burst of MDA production, suggesting the formation of free radicals after diffuse head injury. Even though all the regions sampled show the same effect, certain regions are less affected in this diffuse brain injury animal model.