The Effect Of Glial Fibrillary Acidic Portein In The Rat Spinal Cord Tissue By Limb Ischemic Preconditioning On Spinal Cord Ischemia-reperfusion Injury

Objective:Through investigating the remote preconditioning on spinal cordischemia-reperfusion injury by the expression of gial fibrillary acidic protein in ratsspinal cord tissue,we want to know the influence of gial fibrillary acidic protein inthe spinal cord ischemia-reperfusion injury.Method:Fifty-four male SD rats, weighting250-320grams were randomly divided intothree groups, Sham group（n=6）: after opening the abdominal cavity, expose andseparate the abdominal aorta between the left and right renal artery,then close theabdominal cavity;LIPC group（n=24）: use a tourniquet to block the right lower limbblood flow for10min,then loose the tourniquet10min for reperfusion (do it for2times),30min later,open the abdominal cavity using a noninvasive arterial clipabdominal aorta for30min to build spinal cord ischemia-reperfusion injury model;I/R group（n=24）: establish spinal cord ischemia reperfusion injury model as LIPCgroup. The nerve function score was measured at7d after reperfusion in the Shamgroup and at four time points (6h,1d,3d,7d) after reperfusion in the LIPC and I/Rgroup, then executed the lumbar spinal cord L2-4of rats; Dyeing HE for morphologyand using immunohistochemical method to detection the acidic protein GFAPexpression of glial fibers.Result:Compared with the Sham group, Tarlov scores significantly decreasedespectively at6h,1d,3d after reperfusion in the LIPC group and the I/R group (P <0.05); Compared with I/R group, Tarlov scores increased at6h,1d,3d afterreperfusion in the LIPC group (P <0.05); HE staining showed that neurondegeneration necrosis, vacuolization in I/R group,LIPC group pathological changewas slighter, Sham group was no abnormalities; Compared with the Sham group andthe I/R group, GFAP expression of LIPC group increased, especially at1d,3d afterreperfusion (P <0.05). Conclusion:The remote preconditioning can increase neurologic function score, relievespinal cord ischemia necrosis, increase the expression of GFAP, and relieve spinalcord ischemia-reperfusion injury in rats. The mechanism may be related to theincreasing expression of GFAP and activated astrocytes.