title: Effects of intermittent hypobaric hypoxia preconditioning on the expression of neuroglobin and Bcl-2 in the rat hippocampal CA1 area following ischemia-reperfusion.
abstract: This study was aimed at understanding the effect of intermittent hypobaric hypoxia preconditioning (IHHP) on neuroglobin (NGB) and Bcl-2 expression in the hippocampal CA1 region of rats following global cerebral ischemia-reperfusion. Wistar rats were randomly divided into sham, IHHP control, global cerebral ischemia-reperfusion (IR group), and IHHP+IR groups. The four-vessel occlusion rat model of Pulsinelli was used for the IR groups, in which the common carotid artery was occluded for 8 min before reperfusion. Thionin and immunohistochemical staining were used to observe NGB and Bcl-2 expression in the hippocampal CA1 region. Data was analyzed using the SPSS software. There was a significant increase in the number of surviving cells in the hippocampal CA1 region of the IHHP+IR group (119.5 ± 14) compared to the IR group (41.7 ± 3.8) (P < 0.05). There was a significant increase in the expression of NGB and Bcl-2 in the hippocampal CA1 region of the IHHP+IR group compared to the IR group. By upregulating hippocampal NGB and Bcl-2 expression, IHHP may play a role in neural protection by reducing hippocampal neuronal apoptosis following IR.
authors.affiliation: Pathophysiology Department of Qinghai University Medical College, Xining, Qinghai, China.
authors.forename: Q
authors.initials: Q
authors.lastname: Wu
authors.affiliation: Pathophysiology Department of Qinghai University Medical College, Xining, Qinghai, China.
authors.forename: K X
authors.initials: KX
authors.lastname: Yu
authors.affiliation: Pathophysiology Department of Qinghai University Medical College, Xining, Qinghai, China.
authors.forename: Q S
authors.initials: QS
authors.lastname: Ma
authors.affiliation: Pathophysiology Department of Qinghai University Medical College, Xining, Qinghai, China.
authors.forename: Y N
authors.initials: YN
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002545:Brain Ischemia / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D056547:CA1 Region, Hippocampal / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D002561:Cerebrovascular Disorders / Q000601:surgery; D005786:Gene Expression Regulation; D005914:Globins / Q000819:agonists / Q000235:genetics* / Q000378:metabolism; D000860:Hypoxia; D007150:Immunohistochemistry; D019194:Ischemic Preconditioning / Q000379:methods*; D008297:Male; D009419:Nerve Tissue Proteins / Q000819:agonists / Q000235:genetics* / Q000378:metabolism; D000078787:Neuroglobin; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D010100:Oxygen / Q000494:pharmacology*; D010640:Phenothiazines / Q000737:chemistry; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000819:agonists / Q000235:genetics* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D015398:Signal Transduction
chemical_list: D009419:Nerve Tissue Proteins; D000078787:Neuroglobin; D010640:Phenothiazines; D019253:Proto-Oncogene Proteins c-bcl-2; D005914:Globins; D010100:Oxygen; C009469:thionine