ABSTRACT
Objective:To evaluate the effects of CD34 + cell transplantation on radiation-induced brain injury (RIBI) and the relationship with the activity of astrocytes in rats. Methods:Healthy adult male Sprague-Dawley rats, weighing 210-230 g, were divided into 3 groups ( n=36 each) using a random number table method: control group (C group), RIBI group, and CD34 + group.RIBI model was established by computed tomography (CT) scanning in anesthetized rats.Another 6 rats were selected, and CD34 + cells were eluted by flow cytometry and labeled with BrdU.CD34 + cells were transplanted at day 7 after establishing the model.Brain tissues were obtained at 7, 14 and 28 days after establishing the model in C and RIBI groups and at 14 and 28 days after establishing the model in CD34 + group for determination of Evans blue (EB) extravasation ratio and expression of GFAP (by immuno-histochemistry). Results:Compared with group C, the EB extravasation ratio was significantly increased after establishing the model, and the expression of GFAP was up-regulated in group RIBI ( P<0.05), and no significant change was found in EB extravasation ratio after establishing the model in group CD34 + ( P>0.05). Compared with group RIBI, the EB extravasation ratio was significantly decreased after establishing the model, and the expression of GFAP was down-regulated in group CD34 + ( P<0.05). Conclusion:CD34 + cell transplantation can reduce RIBI, and the mechanism may be related to inhibiting the activity of astrocytes in rats.
ABSTRACT
Objective To explore the dynamic changes of endothelial barrier antigen (EBA) and vascular endothelial growth factor (VEGF) expressions in cerebral cortex under the condition of blood-brain barrier damage in rats following radi?ation-induced brain injury, which provided clinical references. Methods Forty-eight clean grade male SD rats were divid?ed into the control group and 7 d, 14 d, 28 d after brain irradiation group (n=12 for each group) by using stochastic indicator method. The radiation-induced brain injury model was established by using electronic computer X-ray tomography tech?nique. The 3%Evans blue (EB) was injected into rats according to the dose of 3 mL/kg via the tail vein, then the blood ves?sels of cerebral cortex were exposed after having a craniotomy. EB extravasation was detected by microcirculation micro?scope. The permeability of blood-brain barrier was evaluated by using microscope vascular camera device. The expressions of EBA and VEGF in the cerebral cortex were measured by immunohistochemistry staining in each group. Results Both of EB extravasation and VEGF expression in rat cerebral cortex were significantly increased in injury group at day 7, 14 and 28 after brain irradiation compared with those of control group (P<0.05), and which were gradually decreased from day 7 to day 28 after brain irradiation. There were significant differences in EB extravasation and VEGF expression between the injury subgroups (P<0.05). There was a positive correlation between EB extravasation and VEGF expression (r=0.898, P<0.001). The expression levels of EBA were decreased at different time points in injury groups compared with those of control group (P<0.05), and gradually increased from day 7 to 28 after injury. There were significant differences in expression levels of EBA between injury subgroups (P<0.05). The expression of EBA was negatively correlated with EB extravasation (r=-0.866, P<0.001). Conclusion The increases of blood-brain barrier permeability have important relation to the decreases of EBA expression and the increases of VEGF expression after radiation-induced brain injury.
ABSTRACT
The purpose of this study was to test whether oxygen carriers could decrease tissue injury in a rat model of acute myocardial infarct. The study included 3 groups: SD rats in group II and group III were subjected to permanent occlusion of their left anterior descending coronary arteries; SD rats in group I were subjected to sham-operation. The success of modeling was assartained by ECG. Then the rats were given drug via caudal veins for 2 days. A quantitative evaluation was made with an automatic device for interpretation of cardiac troponin T (cTnT); heart staining was made for the calculation of myocardial infarction size (MIS); and myocardial tissue was taken and subjected to routine pathological hematoxylin-eosin (HE) staining for showing myocardial cell injury. cTnT in the sham-operation group was significantly lower by comparison with that in the model group (P < 0.01), and it was slightly lower in the oxygen carriers group than that in the model group, but there was no statistically significant difference (P = 0.18); MIS was significantly smaller in the sham-operation group than that in the model group (P < 0.01), and it was greater in the model rats than that in the oxygen carriers rats (P < 0.05). HE staining of myocardicum in the oxygen carriers group was significantly better than that in the model group (P < 0.01). The evidence suggested that oxygen carriers increased oxygen supply to ischemic myocardium, reduced the myocardial injury, and thus might offer a novel treatment of myocardial infarction.