[Changes of brain p38 MAPK in rabbits with craniocerebral gunshot injury in hot and humid environment].

OBJECTIVE: To study the activation of p38 mitogen-activated protein kinase (MAPK) in the brain of rabbits after craniocerebral gunshot injury in a hot and humid environment (HHE) and explore its possible mechanism. METHODS: Craniocerebral gunshot injury model was established in 30 New Zealand white rabbits, which were subsequently exposed to environment of normal temperature (at 22.0% +/- 0.5 degrees C; with relative humidity of 50%) or HHE at 39.0 +/- 0.5 degrees C; with relative humidity of 80%-85% for 10 min, 30 min, 1 h, 1.5 h, and 2 h groups, respectively, with 5 rabbits in each group. p38 MAPK activity in the brain tissues of the rabbits following the injury and environmental exposure were detected by Western blotting and analyzed semi-quantitatively by Bio-Profil gel image analysis system. RESULTS: p38 MAPK activity in the cortex and hypothalamus was significantly elevated following gunshot injury and HHE exposure, reaching the peak level at 1 h of HHE exposure and then decreased. p38 MAPK activity was significantly higher in the hypothalamus than in the cortex. CONCLUSION: p38 MAPK activity increases in the early stage following craniocerebral gunshot injury and HHE exposure in rabbits, the mechanism of which might involve the secondary brain insult.

[Changes of heat-shock protein 70 in the brain of rabbits with craniocerebral missile injury in hot and humid environment].

OBJECTIVE: To study the changes of heat shock protein 70 (HSP70) in the brain of rabbits with craniocerebral missile injury (CMI) and their impact on the injury in a hot and humid environment (HHE). METHODS: Twenty-four New Zealand white rabbits were randomized into 3 equal groups, namely normal temperature (NT) control group (subjected to treatment at temperature of 22.0+/-0.5 degrees C with relative humidity of 50%), NT gunshot group with CMI and HHE gunshot group with CMI. The rabbits in the latter two groups were subjected to normal temperature of 22.0+/-0.5 degrees C with relative humidity of 50% and environmental temperature of 39.0+/-0.5 degrees C with relative humidity of 80% to 85%, respectively, after establishment of CMI models. HSP70 in the brain tissues and lymphocytes was detected by Western blotting and visualized using chemoluminescence and X-ray films, followed by quantitative gel image analysis. RESULTS: Expressions of HSP70 in the cortex, hypothalamus and lymphocytes increased apparently in HHE gunshot group, and the changes of HSP70 in the lymphocytes were consistent with those in the cerebral cortex and hypothalamus. CONCLUSION: HSP70 expression in the brain tissues and the lymphocytes increase evidently after MCI in HHE.

[Effect of hyperthermia on tight junctions between endothelial cells of the blood-brain barrier model in vitro].

OBJECTIVE: To investigate the effect of hyperthermia in vitro on tight junctions between the endothelial cells of the blood-brain barrier. METHODS: An in vitro blood-brain barrier model was established by coculture of ECV304 cells with astrocytes. Transendothelial resistance (TER) of in vitro blood-brain barrier was determined by Millicell-ERS system, and the morphological change of tight junctions examined by silver staining. The expression level of zonula occluden-1(ZO-1) was analyzed by semi-quantitative reverse transcriptase-PCR. RESULTS: The integrity of tight junctions was disrupted and the expression level of ZO-1 decreased after treatment with hyperthermia. CONCLUSIONS: Tight junctions between the endothelial cells of the blood-brain barrier can be destroyed by hyperthermia, and decreased expression level of ZO-1 induced by hyperthermia is one of the most important molecular mechanisms.