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Objective To study the effect of hypothermia on cerebral mitochondrial respiratory function and ultrastructure after traumatic brain injury(TBI). Methods Sprague-Dawley rats were subjected to moderate brain injury by using lateral fluid-percussion(LFP)and randomly divided into sham operation group,normothermic TBI group(rectal temperature for 36-37℃)and hypothermic TBI group(rectal temperature for 31-32℃ lasting for two hours).The ipsilateral brains were dissected and homogenized brain tissues were extracted to obtain mitochondfia by density-centrifugation and speed-centrifugation at 2,24 hours and at days 3 and 7 after TBI.The mitochondrial uhrastructure was studied by electron microscope.The indices of respiratory control rate(RCR)and P/O ratio of mitochondrial respiratory function were measured after oxygen consumption was determined with a Clark-type electrode.Results The mitochondrial uhrastructure of normothermic TBI group was damaged severely while that of hypothermic TBI group kept relatively integrated.The RCR and P/O ratio were markedly decreased two hours after TBI and reached the lowest level at the 24th hour(P＜0.01).At day 7,RCR kept at a lower level compared with sham operation group but P/O ratio recovered to normal.Change of RCR was similar in hypothermie TBI group and normothermic TBI group.However,RCR of the hypothermic TBI group was significantly higher than that of the normothermic TBI group within three days after TBI.In the meantime,P/O ratio recovered to normal three days after TBI. Conclusion Hypothermia can improve cerebral mitochondrial respiratory function and protect the mitochondrial structure after TBI.
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Objective To observe the morphological changes of dendrite and soma in retinal ganglion cells (RGCs) which subsisted in early diabetic rats. Methods The RGCs of 3-months-course diabetic rats and coeval normal rats were marked by gene gun techniques. To collect RGCs photographs by Leica microscope with Z axis and CCD camera;to observe the changes of diameter, variance of structural features in dendritic field and somata after classification which according to the size and morphology. Thy-1 antibody marks on the retinal RGCs, taking a photograph under fluorescent microscope, counting the changes of retinal RGCs density in early diabetic rat. Results In three-month diabetic rats, the density of retinal RGCs was decreased obviously. Morphological changes of RGCs in the dendritic fields were observed with gene gun technique. There was no severe variation in all kinds of the bole of cell dendrite,in which some only showed crispation partially and sparseness also twisting in the dendritic ramus. The mean diameter of dendritic field and soma in class A of diabetic rats was (401±86)μm, the mean diameter of dendritic field in control group was (315±72) μm,compared with each other, there is statistically significant differences (t=21. 249, P<0. 001), the mean diameter of soma in class A of diabetic rats was (24±6) μm, the mean diameter of soma in control group was (22±5) μm, compared with each other,there is no statistically significant differences (t= 0. 927,P>0.05); the mean diameter of dendritic field and soma in class B of diabetic rats were (170±36). (14±2) μm respectively, in control group were (165±36), (16±2) μm, the mean diameter of dendritic field and soma in class C of diabetic group were (265±78),(17±5) μm respectively, in control group were (251±57),(17±4) μm , compared with each other,there are on statistically significant differences (t=1.357,0.798,0. 835,1.104 ,P>0.05). ConclusionsIn short-term diabetes, the survived RGCs show good plasticity in adult diabetic rats, especially in class A. The changes of dendrites were more sensitive than the soma, which could be the leading index of themorphologic changes of RGCs in the early stage. The good plasticity showed by the RGCs and the time window from changing in dendrite to cell death provide us many evidences not only for the research but also for the nerve protection in clinic.
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Objective:To investigate the effect of rapamycin on renal function and ultrastructure changes after renal ischemia-reperfusion in rats.Methods:Acute ischemic renal injury model was established(right kidney ectomized,45 min of left renal ischemia and reperfusion for 24h).Thirty male Wistar rats were randomly divided into 3 groups:sham operation group(control group or group C,without renal ischemia),renal ischemia-reperfusion group(ischemia-reperfusion group or group I,without rapamycin),renal ischemia-reperfusion and(RPM 4mg/(kg?d)?3d,reperfusion at 2h before the last operation) intravenous injection group(rapamycin group or group U).changes of renal function and renal uhrastructure were measured BUN level,serum creatinine values.Results:Serum creatinine(168?37)?mol/L and BUN concentration(22?6)mmol/L in group I were significantly higher than those in group U:serum creatinine(113?17)?mol/L and BUN concentration(13.8?2.3)mmol/L(P
