Bone marrow mesenchymal stem cells were isolated from C57BL mice, transfected with the cytosine deaminase （CD） gene using a lentivirus vector and co-cultured with C6 glioma cells to verify anti-tumor effects of bone...Bone marrow mesenchymal stem cells were isolated from C57BL mice, transfected with the cytosine deaminase （CD） gene using a lentivirus vector and co-cultured with C6 glioma cells to verify anti-tumor effects of bone marrow mesenchymal stem cells carrying CD genes. C57MSC-CD/eGFP cells converted 5-fluorocytosine to 5-fluorouracil and exhibited significant inhibition of proliferation and apoptosis in C6 glioma cells. C57MSC-CD/eGFP cells were then implanted into rat models of brain C6 glioma. Rats were also intraperitoneally injected with 5-fluorocytosine after 7 days. MSC-CD/eGFP cells were irregularly distributed at the margin of the glioma, as well as encased and reduced the volume of the glioma. CD-transfected bone marrow mesenchymal stem cells inhibit the in vivo growth and in vitro proliferation of glioma.展开更多
Acute ischemic stroke （AIS）, as the third leading cause of death worldwide, is characterized by its high incidence, mortality rate, high incurred disability rate, and frequent reoccurrence. The neuroprotective effec...Acute ischemic stroke （AIS）, as the third leading cause of death worldwide, is characterized by its high incidence, mortality rate, high incurred disability rate, and frequent reoccurrence. The neuroprotective effects of Ginkgo biloba extract （GBE） against several cerebral diseases have been reported in previous studies, but the underlying mechanisms of action are still unclear. Using a novel in vitro rat cortical capillary endothelial cell- astrocyte-neuron network model, we investigated the neuroprotective effects of GBE and one of its important constituents, Ginkgolide B （GB）, against oxygenglucose deprivation/reoxygenation and glucose （OGD/R） injury. In this model, rat cortical capillary endothelial cells, astrocytes, and neurons were cocultured so that they could be synchronously observed in the same system. Pretreatment with GBE or GB increased the neuron cell viability, ameliorated cell injury, and inhibited the cell apoptotic rate through Bax and Bcl-2 expression regulation after OGD/R injury. Furthermore, GBE or GB pretreatment enhanced the transendothelial electrical resistance of capillary endothelial monolayers, reduced the endothelial permeability coefficients for sodium fluorescein （Na-F）, and increased the expression levels of tight junction proteins, namely, ZO-1 and occludin, in endothelial cells. Results demonstrated the preventive effects of GBE on neuronal cell death and enhancement of the function of brain capillary endothelial monolayers after OGD/R injury in vitro; thus, GBE could be used as an effective neuroprotective agent for AIS/reperfusion, with GB as one of its significant constituents.展开更多
基金the Natural Science Foundation of Liaoning Province, No. 20092165a grant from Education Department of Liaoning Province, No. 2008Z081the Science and Technology Development Program of Dalian, No. 2008E13SF203
文摘Bone marrow mesenchymal stem cells were isolated from C57BL mice, transfected with the cytosine deaminase （CD） gene using a lentivirus vector and co-cultured with C6 glioma cells to verify anti-tumor effects of bone marrow mesenchymal stem cells carrying CD genes. C57MSC-CD/eGFP cells converted 5-fluorocytosine to 5-fluorouracil and exhibited significant inhibition of proliferation and apoptosis in C6 glioma cells. C57MSC-CD/eGFP cells were then implanted into rat models of brain C6 glioma. Rats were also intraperitoneally injected with 5-fluorocytosine after 7 days. MSC-CD/eGFP cells were irregularly distributed at the margin of the glioma, as well as encased and reduced the volume of the glioma. CD-transfected bone marrow mesenchymal stem cells inhibit the in vivo growth and in vitro proliferation of glioma.
文摘Acute ischemic stroke （AIS）, as the third leading cause of death worldwide, is characterized by its high incidence, mortality rate, high incurred disability rate, and frequent reoccurrence. The neuroprotective effects of Ginkgo biloba extract （GBE） against several cerebral diseases have been reported in previous studies, but the underlying mechanisms of action are still unclear. Using a novel in vitro rat cortical capillary endothelial cell- astrocyte-neuron network model, we investigated the neuroprotective effects of GBE and one of its important constituents, Ginkgolide B （GB）, against oxygenglucose deprivation/reoxygenation and glucose （OGD/R） injury. In this model, rat cortical capillary endothelial cells, astrocytes, and neurons were cocultured so that they could be synchronously observed in the same system. Pretreatment with GBE or GB increased the neuron cell viability, ameliorated cell injury, and inhibited the cell apoptotic rate through Bax and Bcl-2 expression regulation after OGD/R injury. Furthermore, GBE or GB pretreatment enhanced the transendothelial electrical resistance of capillary endothelial monolayers, reduced the endothelial permeability coefficients for sodium fluorescein （Na-F）, and increased the expression levels of tight junction proteins, namely, ZO-1 and occludin, in endothelial cells. Results demonstrated the preventive effects of GBE on neuronal cell death and enhancement of the function of brain capillary endothelial monolayers after OGD/R injury in vitro; thus, GBE could be used as an effective neuroprotective agent for AIS/reperfusion, with GB as one of its significant constituents.
