| As altitude increasing, air pressure as well as oxygen pressure does decrease. Hypobaric hypoxia has become the main factor of interfering with life activity. As known, central nervous system (CNS) is extremely dependent on aerobic oxidation to supply energy. Hypobaric hypoxia will firstly affect the function of CNS and even threaten the survival. Thereafter it has been an unsettled bottleneck for limiting the organism to adapt at high altitude. How to prevent and repair hypobaric hypoxic injury and how to improve the tolerance ability of CNS to hypoxia is an important question for High Altitude Medicine to answer. Preconditioning possesses a function of self-protection existed ubiquitously in organisms. A pretreatment with mild or moderate temporary stress on the organisms, after an interval, can enforce the ability of adaptation and tolerance of the organisms to subsequent severe permanent stress. We expect that a pretreatment with moderate hypobaric hypoxia on the organisms might induce a preconditioning, which can prevent its neurons from the injury of hypobaric hypoxia. Delayed preconditioning may be achieved through gene expression and protein synthesis. The identification of the genes or proteins during the delayed preconditioning is of very importance for understanding the mechanism and improving the ability of organisms to adapt hypobaric hypoxia. This study aims at uncovering these doubts and suspicions. The study included three parts. In the first part, we investigate the protective role of hypobaric hypoxic pretreatment on hippocampal neurons in BALB /C inbred mice. Hypobaric hypoxic pretreatment was produced in a hypobaric chamber by maintaining a 7000 m altitude above sea level for 2.5 h/d×3d. After 36h, the surviving ability of hippocampal CA1 neurons in the control group and pretreatment group was tested by severe hypobaric hypoxia which was produced by maintaining a 12000 m altitude in a hypobaric chamber for 4 h, by severe ischemia produced by bilateral common carotid artery occlusion for 18 min, by hypobaric hypoxia with ischemia produced by maintaining animals in a hypobaric chamber which pressure equivalent to 8000 m above sea level for 4 h after right lateral carotid artery ligation, and by oxygen glucose deprivation (OGD) in vitro, respectively. Results indicate thathypobaric hypoxic pretreatment can protect hippocampal neurons from severe hypobaric hypoxia, severe ischemia, hypobaric hypoxia with ischemia in vivo and severe OGD in vitro. In this part, we successfully constructed the animal model of delayed preconditioning of hypobaric hypoxia.In the second part, with the combination of SMART PCR cDNA synthesis and SSH techniques, we explore differentially expressed genes between delayed preconditioning and control. According to the animal model constructed, total RNA was isolated from hippocampus. cDNA was synthesized by SMART PCR. cDNA library of differentially expressed gene from the hippocampus in hypobaric hypoxic preconditioning (HHP) (forward) and control (backward) was succeeded in constructing. 452 clones from forward and 74 clones from backward were screened by reverse Northern hybridization. The optical density (OD) of 85 clones were increased by more 2 times in the control than the preconditioning group, while that of 217 clones were increased by that in preconditioning than control, when used subtractive probes. When used unsubtractive probes, OD of 44 clones were increased by above 2 times in control than preconditioning, while that of 135 clones were increased by that in the preconditioning group than the control. 33 clones have been sequenced. Analysis and comparison from the data of GenBank was performed. The similarity of all cDNA is above 95% but one which similarity is 93%. All represent known genes. Mouse cytochrome C oxidase subunit 1, NADH dehydrogenase subunit 1 and 6, DELETED IN SPLIT-HAND/SPLIT-FOOT 1 REGION(DSS1) and cDNA correspond to clone IMAGE: 5251089 of mice cDNA library are increase in hippocampus of HHP mice and that cDNA correspond t...
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