The Artery In The Spinal Cord Of New Zealand Rabbits And The Regulation Mechanism Of TSG-6 On Oxidative Stress After Subarachnoid Hemorrhage In Rats

Part I The arterial supply to the spinal cord in the New ZealandWhite rabbitsObjectiveThe aim of this study was to describe the arterial origination and arrangement of the spinal cord in New Zealand White rabbits.MethodsThe spinal cord arteries of adult New Zealand rabbits were researched by anatomical 10 objects injected with red latex through aorta ascendens and then fixed with 10%formaldehyde.ResultsThe cervical spinal cord region of New Zealand rabbits were supplied by vertebral arteries and posterior inferior cerebellar artery;the thoracic spinal cord region were supplied by the supreme intercostal arteries,intercostal arteries,and subcostal arteries;the lumbar spinal cord region were supplied by lumbar arteries and middle sacral artery;the sacral and coccygeal spinal cord regions were supplied by internal iliac arteries and middle sacral artery.Based on the asymmetry of rediculomedullary arteries,cervical and lumbar anterior rediculomedullary arteries were predominant on the right,but Adamkiewicz artery often originated from the left lumbar artery,and thoracic anterior rediculomedullary arteries on the left.The posterior radiculomedullary arteries had symmetrical distribution between left and right side,and more frequent in cervical or lumbar region than in thoracic region.ConclusionThe arterial origination and arrangement of the spinal cord in New Zealand White rabbits were different than in humans.The variations of arteries should be taken into account if the rabbit was used to establish a spinal cord injury model.Part II The regulation mechanism of TSG-6 on oxidative stress after subarachnoid hemorrhage in ratsBackground:patients with aneurysmal subarachnoid hemorrhage with high morbidity of death,and oxidative stress of early brain injury after subarachnoid hemorrhage play an important role in the process,previous studies have shown that TSG-6 have the function of the inhibition of oxidative stress,this study explore the TSG-6 can control early after subarachnoid hemorrhage oxidative stress reaction,so as to reduce the brain damage.Methods:our experiment object is healthy adult male SD rats(280?320 g),carotid artery puncture the rule of law as a subarachnoid hemorrhage model,after intraventricular injection give TSG-6 recombinant proteins and TSG-6 specific siRNA through the behavior score,brain edema,blood brain barrier damage detection,TUNEL staining and immunofluorescence and immunohistochemistry,Western blot-to assess the degree of brain injury.Results:TSG-6 can relieve cerebral edema after subarachnoid hemorrhage behavioral impairments of blood-brain barrier damage and apoptosis of neurons;TSG-6 increased the expression of ho-1 and bcl-2,and inhibited the expression of Nox2 Bax and Cleaved caspase-3 in brain tissue.TSG-6 specific siRNA may terminate the TSG-6 for subarachnoid hemorrhage after oxidative stress response inhibition andConclusions:TSG-6 can inhibit the activity of Nox2 by increasing the expression of Ho-1 in brain tissue and inhibiting the oxidative stress response in early brain injury after subarachnoid hemorrhage,also inhibits apoptosis proteins Bax and Cleaved the expression of caspase 3,reduce the apoptosis,finally improve the nerve function defect keywords after subarachnoid hemorrhage...