|
Background of ischemic brain injury, also known as ischemic stroke, cerebral infarction, is the obstacle of the blood supply in the brain caused by a variety of reasons, the local brain tissue ischemia, hypoxia, irreversible brain damage occurs. It is the world mortality 2, adult disability a major diseases. Discovery and identification of new treatments, we are faced with the important task. Studies have shown that blood vessel growth regulatory factors such as angiopoietin (Angiopoietin-1, Ang1), by stabilizing the blood-brain barrier (Blood Brain Barrier, BBB) permeability thereby improving ischemic brain injury. As a newly discovered vascular endothelial growth factor ---- the heat shock protein A12B (Heat Shock Protein A12B HSPA12B) is not aware of its role in ischemic brain injury. The to explore HSPA12B ischemic brain injury. Transgenic mice with high expression human HSPA12B gene through the blockage of the left middle cerebral artery (Middle Cerebral Artery Occlusion, MCAO) induced focal cerebral ischemia / reperfusion (Ischemia / Reperfusion, I / R) model, and then observe and to compare expression levels HSPA12B ischemic brain injury in a clear protective effect HSPA12B on ischemic brain injury. Experimental animal models: 8-10 weeks of age HSPA12B transgenic mice (HSPA12B Transgenicmice, HSPA12B Tg) and sex-matched littermates born to wild-type mice (Wild Type, WT), lack of focal cerebral MCAO copy Blood model. Ischemia time of 60 min reperfusion time 3-24h. . Brain damage indicators: (1) in infarct: ischemia 60min / 24h of reperfusion after separation of brain tissue, 2,3,5 - triphenyl tetrazolium (Triphenyltetrazolium Chloride, TTC) staining, photography, Statistical infarct size. (2) Neurological Rating: ischemia 60min / reperfusion 24h, neurobehavioral function test table on the movement of the mouse, touch function evaluation. (3) damage of hippocampal neurons: ischemia 60min / separation of brain tissue into paraffin sections were prepared after 24h of reperfusion, hematoxylin - eosin staining (Hemotoxylin Eosin Staining, HE staining), hippocampus morphology observed under the microscope, nerve element density, and photographed. The blood-brain barrier permeability: ischemic 60min / reperfusion after 3h, the amount of brain tissue penetration over the blood-brain barrier to Evans blue-pass (Evans Blue) (Blood Brain Barrier, BBB) said. Results 1. The high expression HSPA12B significantly reduced MCAO-induced cerebral infarction area. 2. The high expression HSPA12B significant improve MCAO-induced neurological dysfunction. The 3. The high expression HSPA12B significantly mitigate MCAO-induced hippocampal neuronal injury. 4 the high expression HSPA12B significantly reduce MCAO caused by the blood-brain barrier hyperpermeability. Conclusions to express HSPA12B MCAO-induced ischemic brain injury have significant protective effect. However, the exact mechanism remains to be further clarified.
|