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The Neuroprotection of Recombinant Human Granulocyte Colony-Stimulating Factor Given Intranasally to Central Nervous System on Brain Injury Secondary to Subarachnoid Hemorrare

Author: LiangXiao
Tutor: SunBaoLiang
School: Taishan Medical College
Course: Neurology
Keywords: Subarachnoid hemorrhage Recombinant human granulocyte colony- stimulating factor Intranasal administration Cerebral vasospasm Cerebral microcirculation NF-кB Caspase-3 Apoptosis Cerebral protection
CLC: R743.3
Type: Master's thesis
Year: 2010
Downloads: 12
Quote: 0
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Research purposes. Explore through the nose targeting central import recombinant human granulocyte colony-stimulating factor (rhG-CSF) mitigation role of cerebral vasospasm after rat subarachnoid hemorrhage (SAH) (CVS). Explore by nasal targeting central import recombinant human granulocyte colony-stimulating factor (rhG-CSF) on the protective effect of the rat the SAH post-secondary brain injury. Research methods in 24 healthy adult male Wistar rats were randomly divided into four groups (n = 6), namely: normal control group (no treatment), SAH group (hemoglobin solution was added dropwise to the bone window), nasal NS SAH group (half an hour before and detection nasal targeting hub import saline) by the nose of rhG-CSF SAH group (with detection half an hour before nasal targeting hub import equivalent of rhG-CSF) bone window open, revealing the substrate artery, normal to the bone window dropping saline or does not deal with the other groups the dropwise hemoglobin solution. Measuring the diameter of the basilar artery the cycle detection system using a stereo microscope and in vivo; open bone window, revealing leptomeningeal microvascular under the microscope OlymPus biological record leptomeningeal microcirculation. 2 a healthy adult male Wistar rats, using the the autologous arterial cisternals rat SAH model secondary blood injection methods. The rats were randomly divided into normal control group, SAH group, nose NS SAH group, the nose rhG-CSF SAH group, n = 6. Animals in each group in the model after 72 hours of anesthesia, brains were after Transcatheter perfusion fixed, paraffin sections of brain tissue were prepared. Brain stem cross-section, paraffin section, HE staining to observe morphological changes in the basilar artery (BA), BA inner diameter perimeter and wall thickness measured by computer image analysis system; brain coronal paraffin sections using immunohistochemical methods to detect cortical and hippocampal expression of Caspase-3 and the nuclear transcription factor-κB (nuclear factor-KB) protein expression, image acquisition using a stereo microscope, count the number of positive cells; Nissl method to observe the cerebral cortex, hippocampus, choroid plexus, etc. Cell staining and damage, count density of hippocampal CA1 neurons. Research results BA the 1.SAH group and NS SAH and rats were gradually apparent spasm diameter narrowing of serious, compared with the control group, a significant difference (p lt; 0.01); rhG-CSF of SAH rats BA minor spasm diameter narrowing the obvious comparison with the SAH group NS SAH group, a significant difference (p lt; 0.01). Normal control rats leptomeningeal microvascular diameter, blood flow velocity and flow pattern did not change significantly. SAH group and NS SAH group microarteries the gradual emergence of the more obvious the vasoconstriction, flow slowed down, rendering red blood cells to the severe aggregation and \the reverse flow of the artery. rhG-CSF SAH group leptomeningeal microvascular diameter, blood flow velocity and flow pattern than the normal group changed little. 2. (1) HE staining: basilar artery in SAH group and the NS SAH rats significantly cramps, obvious pathological changes vessel wall, vessel wall thickening, luminal narrowing; endothelial cell swelling, deformation, off; internal elastic membrane was tortuous, wrinkles, uneven thickness; intima showed obvious thickening, smooth muscle cell disorder the vascular adventitia visible infiltration of lymphocytes and monocytes; the SAH rats of rhG-CSF basement The artery spasm alleviate wall thickening is not obvious, weakened endothelial wrinkle phenomenon, muscularis and adventitia mild thickening, vascular endothelial cells is slightly swollen, and a small amount of endothelial cell shedding. (2) immunohistochemical technique detected in rat brain tissue to the normal control group of Caspase-3 protein NF-kb, see a very small amount of expression; NF-kb in SAH group and the NS SAH rats brain tissue, caspase-3 protein The number of positive cells was significantly increased, but the positive cell count was no significant difference; rhG-CSF SAH group rats NF-kb, Caspase-3 protein positive cells decreased compared with the the SAH group NS SAH group. (3) Nissl staining normal control group rat hippocampal CA1 neurons deeply stained neurons were observed, the more the number of cells, arranged in neat rows, cytoplasm Nissl bodies; in SAH group and the NS SAH rats group hippocampal CA1 neurons arrangement is reduced compared to the disorder, the number of cells, the majority of neuron cell body swelling, cell body becomes irregular, cytoplasm vacuolization, nuclear condensation, chromatin margination; pyramidal cells shrinkage, cell pyknosis, triangular, the staining shallow Nissl bodies in the cytoplasm of a decrease in the number or disappear; rhG-CSF SAH group rat neuronal injury to a lesser extent, Nissl bodies increased significantly, stained dark. Research conclusions. Nasal targeting central import rhG-CSF can alleviate the basilar artery spasm after SAH; improve the leptomeningeal microcirculation, increase blood supply to the brain, after SAH basilar artery acute and delayed cerebrovascular spasm and microarteries The cramps have the obvious relief role. Can reduce nasal targeting central import rhG-CSF-induced apoptotic protein Caspase-3 positive cells decreased expression of neuronal apoptosis after anti-SAH secondary ischemic injury; inhibition of NF-κB activation and inhibition of inflammation reaction, reducing neuronal damage, and thus play a protective effect of secondary cerebral ischemic injury after SAH.

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CLC: > Medicine, health > Neurology and psychiatry > Neurology > Cerebrovascular disease > Acute cerebrovascular disease ( stroke)
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