| Objective:To investigate the protective effect of Apelin-13on isehemia-reperfused injury and explore the possible mechanisms in the focal cerebral isehemia-reperfused rats.Methods:The rats models with right focal middle cerebral artery ischemia-reperfusion were established by filament in Sprague Dawley (S-D) male rats. After2hour ischemia the rata were followed by72hour reperfusion. Apelin-13(0.1,1.0and10.0μg/kg) was administered by intracerebroventricular injection15minutes before reperfusion. The score of neural function defect was completed in different after operation. The2,3,5-three phenyl tetrazolium chloride dye was used to calculate the volume and rate of cerebral infarction. The pathological structure of brain tissue was observated by H-E dyeing. The tissue bomogenate of brain tissue in the surrounding area of ischemia was prepared. The level of malondialdehyde (MDA), the activity of superoxide dismutase (SOD) and the level of reactive oxygen species (ROS) in the tissue bomogenate of brain tissue were measured by spectrophotography. The level of total antioxidant capacity (T-AOC) in the tissue bomogenate of brain tissue was tested by double antibody sandwich method assay. The level of reduced glutathione hormon (GSH) in the tissue bomogenate of brain tissue was measured by ELISA assay. The mRNA and protein expressions of BDNF and TrkB of brain tissue in the surrounding area of ischemia were measured by Real-time PCR and Western blot respectively.Results:(1) Compared with the ischemia-reperfusion group, the neural function defect was significantly improved, muscle strength was significantly enhanced and the score of neural function defect was significantly decreased in dose dependent manner in the Apelin-13(1.0and10.0μg/kg) group (all P<0.05).(2) Compared with the ischemia-reperfusion group, the water content of brain tissue, the volume and rate of infarct were significantly decreased in dose dependent manner in the Apelin-13(1.0and10.0μg/kg) group (all P<0.05).(3) The structure of brain of rats was normal, the nucleus of neuron was located in the centre of cells, the degeneration and necrosis of neuron were not observated in the sham group. Compared with the sham group, the amount of neuron was significantly decreased in the ischemia-reperfusion group. The tissue edema, the degeneration and necrosis of neuron, the karyopyknosis and caryolysis of nucleus were observated in the ischemia-reperfusion group. Compared with the ischemia-reperfusion group, the structure of brain of rats was improved, the degree of edema, karyopyknosis and caryolysis of nucleu were significantly decreased and the amount of degeneration and necrosis of neuron were significantly decreased in the Apelin-13(1.0and10.0μg/kg) group.(4) Compared with the ischemia-reperfusion group, the level of MDA and the level of ROS in the tissue bomogenate of brain tissue in the surrounding area of ischemia were significantly decreased in dose dependent manner in the Apelin-13(1.0and10.0μg/kg) group (all P<0.05); the level of T-AOC, the activity of SOD and the level of GSH in the tissue bomogenate of brain tissue in the surrounding area of ischemia were significantly increased in dose dependent manner in the Apelin-13(1.0and10.0μg/kg)(all P<0.05).(5) Compared with the ischemia-reperfusion group, the mRNA and protein expressions of BDNF and TrkB of brain tissue in the surrounding area of ischemia were significantly up-regulated in dose dependent manner in the Apelin-13(1.0and10.0μg/kg)(all P<0.05).Conclusion:Apelin-13protects the ischemia-reperfusion injury, which the mechanisms may be related with the inhibition of oxidative stress and up-regulation of BDNF and TrkB induced by Apelin-13.12figures,1tables,73references. |
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