2010Chinese Journal of NeonatologyRequires access

Study on the protective effect and mechanism of hypoxic preconditioning on the brain in rats after hypoxic-ischemic brain damage

Yin Xian-mi

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Abstract

Objective To explore the protective effect and mechanism of hypoxic preconditioning on the brain in SD rats after hypoxic-ischemic brain damage(HIBD). Methods Forty-eight seven-day-old SD rats were used and divided into 4 groups randomly:control group,sham operation group,HIBD group and HIBD +hypoxic preconditioning group (HPC). HPC model was established by exposure a humidified gas mixture of 8% oxygen/92% nitrogen at an approximate flow rate of 0.3 L/min. With the research methods and techniques of immunofluorescence and confocal laser scanning,microscope measurement of cell apoptosis,fluorescence intensity of Bcl-2 and Caspase-3 in cortex and hippocampus was done respectively. Results More TUNEL stained positive cells could be found in HIBD group and HIBD+HPC group than those in sham operation group (P0.05). TUNEL stained positive cells decreased rapidly in HIBD+HPC group than those in HIBD group (P0.05). Fluorescence intensity of Bcl-2 and Caspase-3 was faint in control group and sham operation group,and there was no difference between them (P0.05). The expression of Bcl-2 and Caspase-3 in both HIBD group and HIBD+HPC group was higher than that in sham operation group. The expression of Bcl-2 in HIBD+HPC group was even higher than that in HIBD group,whereas the expression of Caspase-3 in HIBD+HPC was significantly lower than that in HIBD (P0.05). Conclusion Apoptosis of cortex and hippocampus cells in SD rats after HIBD is resisted via increased expression of Bcl-2 and lowered activity of Caspase-3 in the cortex and hippocampus,and brain cells are thereby protected during hypoxic preconditioning.

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Objective To explore the protective effect and mechanism of hypoxic preconditioning on the brain in SD rats after hypoxic-ischemic brain damage(HIBD). Methods Forty-eight seven-day-old SD rats were used and divided into 4 groups randomly:control group,sham operation group,HIBD group and HIBD +hypoxic preconditioning group (HPC). HPC model was established by exposure a humidified gas mixture of 8% oxygen/92% nitrogen at an approximate flow rate of 0.3 L/min. With the research methods and techniques of immunofluorescence and confocal laser scanning,microscope measurement of cell apoptosis,fluorescence intensity of Bcl-2 and Caspase-3 in cortex and hippocampus was done respectively. Results More TUNEL stained positive cells could be found in HIBD group and HIBD+HPC group than those in sham operation group (P0.05). TUNEL stained positive cells decreased rapidly in HIBD+HPC group than those in HIBD group (P0.05). Fluorescence intensity of Bcl-2 and Caspase-3 was faint in control group and sham operation group,and there was no difference between them (P0.05). The expression of Bcl-2 and Caspase-3 in both HIBD group and HIBD+HPC group was higher than that in sham operation group. The expression of Bcl-2 in HIBD+HPC group was even higher than that in HIBD group,whereas the expression of Caspase-3 in HIBD+HPC was significantly lower than that in HIBD (P0.05). Conclusion Apoptosis of cortex and hippocampus cells in SD rats after HIBD is resisted via increased expression of Bcl-2 and lowered activity of Caspase-3 in the cortex and hippocampus,and brain cells are thereby protected during hypoxic preconditioning.

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Available abstract

Objective To explore the protective effect and mechanism of hypoxic preconditioning on the brain in SD rats after hypoxic-ischemic brain damage(HIBD). Methods Forty-eight seven-day-old SD rats were used and divided into 4 groups randomly:control group,sham operation group,HIBD group and HIBD +hypoxic preconditioning group (HPC). HPC model was established by exposure a humidified gas mixture of 8% oxygen/92% nitrogen at an approximate flow rate of 0.3 L/min. With the research methods and techniques of immunofluorescence and confocal laser scanning,microscope measurement of cell apoptosis,fluorescence intensity of Bcl-2 and Caspase-3 in cortex and hippocampus was done respectively. Results More TUNEL stained positive cells could be found in HIBD group and HIBD+HPC group than those in sham operation group (P0.05). TUNEL stained positive cells decreased rapidly in HIBD+HPC group than those in HIBD group (P0.05). Fluorescence intensity of Bcl-2 and Caspase-3 was faint in control group and sham operation group,and there was no difference between them (P0.05). The expression of Bcl-2 and Caspase-3 in both HIBD group and HIBD+HPC group was higher than that in sham operation group. The expression of Bcl-2 in HIBD+HPC group was even higher than that in HIBD group,whereas the expression of Caspase-3 in HIBD+HPC was significantly lower than that in HIBD (P0.05). Conclusion Apoptosis of cortex and hippocampus cells in SD rats after HIBD is resisted via increased expression of Bcl-2 and lowered activity of Caspase-3 in the cortex and hippocampus,and brain cells are thereby protected during hypoxic preconditioning.

Key concepts: Brain damage, TUNEL assay, Apoptosis, Medicine, Hippocampus, Caspase 3, Hypoxia (environmental), Molecular biology

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