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| 1 | Morphological properties and proliferation analysis of olfactory ensheathing cells seeded onto three-dimensional collagen-heparan sulfate biological scaffolds显示文摘This study aimed to examine the differences in the morphological properties and proliferation of ol-factory ensheathing cells in three-dimensional culture on collagen-heparan sulfate biological scaf-folds and in two-dimensional culture on common flat culture plates.The proliferation rate of olfactory ensheathing cells in three-dimensional culture was higher than that in two-dimensional culture,as detected by an MTT assay.In addition,more than half of the olfactory ensheathing cells subcultured using the trypsinization method in three-dimensional culture displayed a spindly Schwann cell-like morphology with extremely long processes,while they showed a flat astrocyte-like morphology in two-dimensional culture.Moreover,spindle-shaped olfactory ensheathing cells tended to adopt an elongated bipolar morphology under both culture conditions.Experimental findings indicate that the morphological properties and proliferation of olfactory ensheathing cells in three-dimensional culture on collagen-heparan sulfate biological scaffolds are better than those in two-dimensional culture. | Na Liu Zhouping Tang Zhiyuan Yu Minjie Xie Yu Zhang Erfang Yang Shabei Xu | 2012 | Neural Regeneration Research2012，7，16： | 2 |
| 2 | Reactive changes in astrocytes, and delayed neuronal death, in the rat hippocampal CA1 region following cerebral ischemia/reperfusion显示文摘BACKGROUND: Blood supply to the hippocampus is not provided by the middle cerebral artery. However, previous studies have shown that delayed neuronal death in the hippocampus may occur following focal cerebral ischemia induced by middle cerebral artery occlusion. OBJECTIVE: To observe the relationship between reactive changes in hippocampal astrocytes and delayed neuronal death in the hippocampal CA1 region following middle cerebral artery occlusion. DESIGN, TIME AND SETTING: The immunohistochemical, randomized, controlled animal study was performed at the Laboratory of Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, from July to November 2007. MATERIALS: Rabbit anti-glial fibrillary acidic protein (GFAP) (Neomarkers, USA), goat anti-rabbit IgG (Sigma, USA) and ApoAlert apoptosis detection kit (Biosciences Clontech, USA) were used in this study. METHODS: A total of 42 healthy adult male Wistar rats, aged 3–5 months, were randomly divided into a sham operation group (n = 6) and a cerebral ischemia/reperfusion group (n = 36). In the cerebral ischemia/reperfusion group, cerebral ischemia/reperfusion models were created by middle cerebral artery occlusion. In the sham operation group, the thread was only inserted into the initial region of the internal carotid artery, and middle cerebral artery occlusion was not induced. Rats in the cerebral ischemia/reperfusion group were assigned to a delayed neuronal death (+) subgroup and a delayed neuronal death (–) subgroup, according to the occurrence of delayed neuronal death in the ischemic side of the hippocampal CA1 region following cerebral ischemia. MAIN OUTCOME MEASURES: Delayed neuronal death in the hippocampal CA1 region was measured by Nissl staining. GFAP expression and delayed neuronal death changes were measured in the rat hippocampal CA1 region at the ischemic hemisphere by double staining for GFAP and TUNEL. RESULTS: After 3 days of ischemia/reperfusion, astrocytes with abnormal morphology were detected in the rat hippocampal CA1 region in the delayed neuronal death (+) subgroup. No significant difference in GFAP expression was found in the rat hippocampal CA1 region at the ischemic hemisphere in the sham operation group, delayed neuronal death (+) subgroup and delayed neuronal death (–) subgroup (P > 0.05). After 7 days of ischemia/reperfusion, many GFAP-positive cells, which possessed a large cell body and an increased number of processes, were activated in the rat hippocampal CA1 region at the ischemic hemisphere. GFAP expression in the hippocampal CA1 region was greater in the delayed neuronal death (+) subgroup and delayed neuronal death (–) subgroup compared with the sham operation group (P < 0.01). Moreover, GFAP expression was significantly greater in the delayed neuronal death (–) subgroup than in the delayed neuronal death (+) subgroup (P < 0.01). After 30 days of ischemia/reperfusion, GFAP-positive cells were present in scar-like structures in the rat hippocampal CA1 region at the ischemic hemisphere. GFAP expression was significantly greater in the delayed neuronal death (+) subgroup and delayed neuronal death (–) subgroup compared with the sham operation group (P < 0.05). GFAP expression was significantly lower in the delayed neuronal death (–) subgroup than in the delayed neuronal death (+) subgroup (P < 0.05). The delayed neuronal death rates were 42% (5/12), 33% (4/12) and 33% (4/12) at 3, 7 and 30 days, respectively, followingischemia/reperfusion. No significant differences were detected at various time points (χ2 = 0.341, P > 0.05). CONCLUSION: The activation of astrocytes was poor in the hippocampal CA1 region during the early stages of ischemia, which is an important reason for delayed neuronal death. Glial scar formation aggravated delayed neuronal death during the advanced ischemic stage. | Guiqing Zhang Xiang Luo Zhiyuan Yu Chao Ma Shabei Xu Wei Wang | 2009 | Neural Regeneration Research2009，4，1： | 2 |
| 3 | Cortical and Subcortical Grey Matter Abnormalities in White Matter Hyperintensities and Subsequent Cognitive Impairment显示文摘Grey matter(GM)alterations may contribute to cognitive decline in individuals with white matter hyperintensities(WMH)but no consensus has yet emerged.Here,we investigated cortical thickness and grey matter volume in 23 WMH patients with mild cognitive impairment(WMH-MCI),43 WMH patients without cognitive impairment,and 55 healthy controls.Both WMH groups showed GM atrophy in the bilateral thalamus,fronto-insular cortices,and several parietal-temporal regions,and the WMH-MCI group showed more extensive and severe GM atrophy.The GM atrophy in the thalamus and fronto-insular cortices was associated with cognitive decline in the WMH-MCI patients and may mediate the relationship between WMH and cognition in WMH patients.Furthermore,the main results were well replicated in an independent dataset from the Alzheimer's Disease Neuroimaging Initiative database and in other control analyses.These comprehensive results provide robust evidence of specific GM alterations underlying WMH and subsequent cognitive impairment. | Wenhao Zhu Hao Huang Shiqi Yang Xiang Luo Wenzhen Zhu Shabei Xu Qi Meng Chengchao Zuo Yong Liu Wei Wang Alzheimer’s Disease Neuroimaging Initiative | 2021 | Neuroscience Bulletin2021，37，6： | 1 |
| 4 | Biocompatibility of a collagen-heparin sulfate scaffold implanted into porcine brain显示文摘BACKGROUND: Collagen-heparin sulfate scaffolds have been widely used to repair nerve injury and promote nerve regeneration. Previous research has evaluated scaffold biocompatibility by measuring gliocyte proliferation but not neuronal apoptosis. OBJECTIVE: To explore the biocompatibility of collagen-heparin sulfate scaffold in porcine brain by detecting peripheral neural apoptosis and protein expression. DESIGN, TIME AND SETTING: A randomized, controlled animal experiment was performed at the Laboratory of Neurology, Tongji Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, between March and June, 2008. MATERIALS: Rabbit anti-human Bax, Caspase-3 polyclonal antibody, rat anti-human Bcl-2 polyclonal antibody, streptavidin biotin-peroxidase complex (SABC) immunohistochemical kit, and TUNEL kit (Roche, USA) were used in this study. METHODS: Twenty adult piglets were randomly evenly divided into implantation and control groups. A collagen-heparin sulfate scaffold was implanted from the anterior fontanelle into the brain in the implantation group. The same puncture but no scaffold implantation was made in the control group. MAIN OUTCOME MEASURES: Cell apoptosis was detected using TUNEL; Bax, Bcl-2, and Caspase-3 expressions were measured using the SABC method. RESULTS: At days 1, 3, 7, and 14 after scaffold implantation, a few apoptotic cells were observed in the brain tissues near the puncture site, with more apoptotic cells in the implantation group (P < 0.05). However, both groups showed similar apoptosis levels by day 30 after implantation. Implan-tation increased Bax, Bcl-2, and Caspase-3 expressions on days 3 and 7 after implantation (P < 0.05) but decreased the ratio of Bcl-2 to Bax in the implantation group was significantly lower on days 3 and 7 (P < 0.05), with no significant difference by day 30 after implantation (P > 0.05). CONCLUSION: The collagen-heparin sulfate scaffold has good biocompatibility to porcine brain tissues. | Zhouping Tang Xingyong Chen Wengao Zeng Shabei Xu Xuewei Xie Ronghua Tang Suiqiang Zhu | 2010 | Neural Regeneration Research2010，5，3： | 0 |
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