title: The experiment research of neuroprotection of hypoperfusion postconditioning on cerebral ischemia.
abstract: In this study, we tested the hypothesis that the alternating of hypoperfusion and full reperfusion (hypoperfusion postconditioning) could improve neuroprotection on cerebral ischemia in rats and explored the role of TAp63 and △Np63 in this process. Eighty male Sprague Dawley rats were randomly divided into 4 groups: the sham group, the cerebral ischemic/reperfusion group (I/R), the hypoperfusion group 1 (HR1), and the hypoperfusion group 2 (HR2). Cerebral ischemia was established by clamping the bilateral common carotid artery with hypotension for 20 minutes. For the rats in the HR1 group, the blood pressure was maintained to 80 to 90 mm Hg in clamping bilateral common carotid artery minutes and then unclamped. For the rats in the HR2 group, the clamping was performed at one side of the common carotid artery and one half of the other side of common carotid artery. Neurologic behavior scores in the I/R, HR1, and HR2 groups decreased significantly after cerebral ischemia, and scores in the HR2 group were significantly higher than those in the I/R group (P < 0.05). Neuronal densities in the HR1 and HR2 groups were significantly higher than that in the I/R group (P < 0.05). Neuronal apoptosis in the HR1 and HR2 groups was significantly lower than that in the I/R group (P < 0.05). TAp63 and S100β concentration decreased, and △Np63 increased significantly in the HR1 and HR2 groups as compared with the I/R group (P < 0.05). No significant difference in these parameters between the HR1 and HR2 groups (P > 0.05). Alternating of hypoperfusion and normal perfusion postconditioning had neuroprotection function on cerebral ischemia in the rats. This could relate with decreasing expression of TAp63 and increasing expression of △Np63 in hippocampal region of the first area in the hippocampal circuit to inhibit neuronal apoptosis.
authors.affiliation: From the *Department of Pain and Anesthesiology, Affiliated Hospital of Luzhou Medical College, Luzhou; †Department of Anesthesiology, Fourth People's Hospital of Zigong City, Zigong, Sichuan; and ‡Department of Anesthesiology, Chinese Medicine Hospital of Lianyungang City, Lianyungang City, Jiangsu, China.
authors.forename: Changhe
authors.initials: C
authors.lastname: Ren
authors.forename: Xuan
authors.initials: X
authors.lastname: Yu
authors.forename: Gangming
authors.initials: G
authors.lastname: Wu
authors.forename: Changli
authors.initials: C
authors.lastname: Liao
authors.forename: Qiao
authors.initials: Q
authors.lastname: Tang
authors.forename: Jian
authors.initials: J
authors.lastname: Zhan
authors.forename: Cehua
authors.initials: C
authors.lastname: Ou
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001522:Behavior, Animal; D001794:Blood Pressure / Q000502:physiology; D002545:Brain Ischemia / Q000517:prevention & control*; D002452:Cell Count; D006624:Hippocampus / Q000737:chemistry / Q000473:pathology; D007022:Hypotension / Q000503:physiopathology; D057775:Ischemic Postconditioning / Q000379:methods*; D008297:Male; D009048:Motor Skills / Q000502:physiology; D009474:Neurons / Q000473:pathology; D010146:Pain / Q000503:physiopathology; D010750:Phosphoproteins / Q000032:analysis; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000517:prevention & control*; D009418:S100 Proteins / Q000032:analysis; D012903:Smell / Q000502:physiology; D012919:Social Behavior; D025521:Tumor Suppressor Proteins / Q000032:analysis; D014785:Vision, Ocular / Q000502:physiology
chemical_list: D010750:Phosphoproteins; D009418:S100 Proteins; D025521:Tumor Suppressor Proteins