Objective To investigate the effect of glutamine(Gln)on the content of reduced glutathione hormone(GSH)and aminoglutaminic acid(Glu)of spinal cord following ischemia-reperfusion injury.Methods Totally 40 healthy adult...Objective To investigate the effect of glutamine(Gln)on the content of reduced glutathione hormone(GSH)and aminoglutaminic acid(Glu)of spinal cord following ischemia-reperfusion injury.Methods Totally 40 healthy adult male rabbits were randomly divided into five groups:sham-operation group(S group),ischemia-reperfusion injury group(I/R group),low-dose glutamine group(L Gln group),median-dose glutamine group(M Gln group)and high-dose glutamine group(H Gln group).After glutamine preconditioning,the model of spinal cord ischemia-reperfusion injury was established according to Zivin’s method.The general status of animals was observed and the changes of Jacobs scoring were recorded in each group.Malondialdehydes(MDA),GSH,Glu and superoxide dismutase(SOD)activity in lumbar spinal cord tissues were determined using chemical colorimetry.The neuron number and deviation rate in spinal cord anterior horn were observed histopathologically.Results There was no significant difference between L Gln group and I/R group in behavior scoring,SOD activity,content of MDA and Glu,neuron number and deviation rate of spinal cord(P>0.05);however,there was a significant difference in GSH content of spinal cord(P<0.05).M Gln group and I/R group differed significantly(P<0.05)in behavior scoring,SOD activity,content of MDA,Glu,GSH,neuron number and deviation rate of spinal cord.Between H Gln group and M Gln group,there was no significant difference in behavior scoring,content of MDA and Glu,SOD activity,neuron number and aberration rate in spinal cord(P>0.05),whereas there was a significant difference in SOD activity and Glu content(P<0.05).Conclusion Pretreatment with medium-dose glutamine has a protective effect on spinal cord ischemia-reperfusion injury in rabbits,which may be related to the maintenance of GSH content,increase of SOD activity and reduction of MDA.展开更多
AIM： To investigate the potential of pigment epitheliumderived factor（PEDF） to protect the immortalized rat retinal ganglion cells-5（RGC-5） exposed to Co Cl2-induced chemical hypoxia. METHODS： After being differ...AIM： To investigate the potential of pigment epitheliumderived factor（PEDF） to protect the immortalized rat retinal ganglion cells-5（RGC-5） exposed to Co Cl2-induced chemical hypoxia. METHODS： After being differentiated with staurosporine（SS）, RGC-5 cells were cultured in four conditions： control group cells cultured in Dulbecco ＇s modified eagle medium（DMEM） supplemented with 10% fetal bovine serum, 100 μmol/m L streptomycin and penicillin（named as normal conditions）; hypoxia group cells cultured in DMEM containing 300 μmol/m L Co Cl2; cells in the group protected by PEDF were first pretreated with 100 ng/m L PEDF for 2h and then cultured in the same condition as hypoxia group cells; and PEDF group cells that were cultured in the presence of 100 ng/m L PEDF under normal conditions. The cell viability was assessed by MTT assay, the percentage of apoptotic cells was quantified using Annexin V-FITC apoptosis kit, and intra-cellar reactive oxygen species（ROS） was measured by dichloro-dihydro-fluorescein diacetate（DCFH-DA） probe. The mitochondria-mediated apoptosis was also examined to further study the underlying mechanism of the protective effect of PEDF. The opening of mitochondrial permeability transition pores（m PTPs） and membrane potential（Δψm） were tested as cellular adenosine triphosphate（ATP） level and glutathione（GSH）. Also, the expression and distribution of Cyt C and apoptosis inducing factor（AIF） were observed.RESULTS： SS induced differentiation of RGC-5 cells resulting in elongation of their neurites and establishing contacts between outgrowths. Exposure to 300 μmol/m L Co Cl2 triggered death of 30% of the total cells in cultures within 24 h. At the same time, pretreatment with 100 ng/m L PEDF significantly suppressed the cell death induced by hypoxia（P〈0.05）. The apoptosis induced by treatment of Co Cl2 was that induced cell death accompanied with increasing intracellar ROS and decreasing GSH and ATP level. PEDF pretreatment suppresse展开更多
文摘Objective To investigate the effect of glutamine(Gln)on the content of reduced glutathione hormone(GSH)and aminoglutaminic acid(Glu)of spinal cord following ischemia-reperfusion injury.Methods Totally 40 healthy adult male rabbits were randomly divided into five groups:sham-operation group(S group),ischemia-reperfusion injury group(I/R group),low-dose glutamine group(L Gln group),median-dose glutamine group(M Gln group)and high-dose glutamine group(H Gln group).After glutamine preconditioning,the model of spinal cord ischemia-reperfusion injury was established according to Zivin’s method.The general status of animals was observed and the changes of Jacobs scoring were recorded in each group.Malondialdehydes(MDA),GSH,Glu and superoxide dismutase(SOD)activity in lumbar spinal cord tissues were determined using chemical colorimetry.The neuron number and deviation rate in spinal cord anterior horn were observed histopathologically.Results There was no significant difference between L Gln group and I/R group in behavior scoring,SOD activity,content of MDA and Glu,neuron number and deviation rate of spinal cord(P>0.05);however,there was a significant difference in GSH content of spinal cord(P<0.05).M Gln group and I/R group differed significantly(P<0.05)in behavior scoring,SOD activity,content of MDA,Glu,GSH,neuron number and deviation rate of spinal cord.Between H Gln group and M Gln group,there was no significant difference in behavior scoring,content of MDA and Glu,SOD activity,neuron number and aberration rate in spinal cord(P>0.05),whereas there was a significant difference in SOD activity and Glu content(P<0.05).Conclusion Pretreatment with medium-dose glutamine has a protective effect on spinal cord ischemia-reperfusion injury in rabbits,which may be related to the maintenance of GSH content,increase of SOD activity and reduction of MDA.
基金Supported by National Natural Science Foundation of China(No.81100665)
文摘AIM： To investigate the potential of pigment epitheliumderived factor（PEDF） to protect the immortalized rat retinal ganglion cells-5（RGC-5） exposed to Co Cl2-induced chemical hypoxia. METHODS： After being differentiated with staurosporine（SS）, RGC-5 cells were cultured in four conditions： control group cells cultured in Dulbecco ＇s modified eagle medium（DMEM） supplemented with 10% fetal bovine serum, 100 μmol/m L streptomycin and penicillin（named as normal conditions）; hypoxia group cells cultured in DMEM containing 300 μmol/m L Co Cl2; cells in the group protected by PEDF were first pretreated with 100 ng/m L PEDF for 2h and then cultured in the same condition as hypoxia group cells; and PEDF group cells that were cultured in the presence of 100 ng/m L PEDF under normal conditions. The cell viability was assessed by MTT assay, the percentage of apoptotic cells was quantified using Annexin V-FITC apoptosis kit, and intra-cellar reactive oxygen species（ROS） was measured by dichloro-dihydro-fluorescein diacetate（DCFH-DA） probe. The mitochondria-mediated apoptosis was also examined to further study the underlying mechanism of the protective effect of PEDF. The opening of mitochondrial permeability transition pores（m PTPs） and membrane potential（Δψm） were tested as cellular adenosine triphosphate（ATP） level and glutathione（GSH）. Also, the expression and distribution of Cyt C and apoptosis inducing factor（AIF） were observed.RESULTS： SS induced differentiation of RGC-5 cells resulting in elongation of their neurites and establishing contacts between outgrowths. Exposure to 300 μmol/m L Co Cl2 triggered death of 30% of the total cells in cultures within 24 h. At the same time, pretreatment with 100 ng/m L PEDF significantly suppressed the cell death induced by hypoxia（P〈0.05）. The apoptosis induced by treatment of Co Cl2 was that induced cell death accompanied with increasing intracellar ROS and decreasing GSH and ATP level. PEDF pretreatment suppresse
