Fei Xie1, Rui Xu1, Xue Song1, Haiyuan Zhu1, Xin Wang2, Ji Zhu1. 1. Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University Chongqing 400016, China. 2. Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School Boston, Massachusetts 02115, USA.
Abstract
OBJECTIVE: To investigate the joint protective effect of exogenous neuroglobin (Ngb) and hemin on ischemic brain tissue in rats and its possible mechanisms. METHODS: Sprague Dawley rats (n = 175) were randomly divided into five groups (n = 35): sham, ischemia, hemin intervention, Ngb plasmid intervention, and hemin and plasmid joint intervention. The classic MCAO rat model of focal cerebral ischemia was used. After recovery from anaesthesia, neurobehavioral testing was performed. The following factors were measured 24 hours post-surgery: brain water content, infarct volume ratio, neuron apoptosis detected by in situ cell apoptosis technology (TUNEL), Bcl-2 protein expression detected by immunofluorescence, and Ngb and Bcl-2 protein expression analyzed by western blot. RESULTS: In the Ngb plasmid and hemin joint intervention group, there were significant reductions (i.e., improvements) in neurobehavioral scores, brain water content, and infarct volume ratio. The reduction of the number of apoptotic neurons and the increase in Ngb protein and Bcl-2 protein expression in this group were both significantly different from the sham group (P < 0.05). CONCLUSION: In the event of focal cerebral ischemia in rats, the joint action of exogenous Ngb and hemin could strengthen the inhibition of cell apoptosis, which achieves its protection effect on ischemic brain tissues, possibly by up-regulating Bcl-2 protein expression.
OBJECTIVE: To investigate the joint protective effect of exogenous neuroglobin (Ngb) and hemin on ischemic brain tissue in rats and its possible mechanisms. METHODS:Sprague Dawley rats (n = 175) were randomly divided into five groups (n = 35): sham, ischemia, hemin intervention, Ngb plasmid intervention, and hemin and plasmid joint intervention. The classic MCAOrat model of focal cerebral ischemia was used. After recovery from anaesthesia, neurobehavioral testing was performed. The following factors were measured 24 hours post-surgery: brain water content, infarct volume ratio, neuron apoptosis detected by in situ cell apoptosis technology (TUNEL), Bcl-2 protein expression detected by immunofluorescence, and Ngb and Bcl-2 protein expression analyzed by western blot. RESULTS: In the Ngb plasmid and hemin joint intervention group, there were significant reductions (i.e., improvements) in neurobehavioral scores, brain water content, and infarct volume ratio. The reduction of the number of apoptotic neurons and the increase in Ngb protein and Bcl-2 protein expression in this group were both significantly different from the sham group (P < 0.05). CONCLUSION: In the event of focal cerebral ischemia in rats, the joint action of exogenous Ngb and hemin could strengthen the inhibition of cell apoptosis, which achieves its protection effect on ischemic brain tissues, possibly by up-regulating Bcl-2 protein expression.
Authors: Yi Zhang; Xin Wang; Sergei V Baranov; Shan Zhu; Zhihong Huang; Wendy Fellows-Mayle; Jiying Jiang; Arthur L Day; Bruce S Kristal; Robert M Friedlander Journal: Neurosurgery Date: 2011-10 Impact factor: 4.654