This study was performed to assess the effect of myocardial ischemicreperfusion on cardiac function and research the action of free radicals in the reperfusion injury by observing the effect of free radical scavenger (superoxide dismutase, SOD) in the shortly ischemic-reperfused rabbits. Three groups were studied: Group Ⅰ (SOD 300u/kg, n= 10) and Group Ⅱ (control, n= 8) were subjected to 15 rain of total occlusion of the left ventricular branch of coronary artery (LVB) followed by 10 min of reperfusion; in Group Ⅲ (n= 8), rabbits underwent continuous occlusion of LVB for 25 min. Cardiac index (CI), left ventricutar systolic peak pressure (LVSP), maximum rate of left ventricular pressure development (+dp/dr max), and maximum rate of fall of left ventricular pressure (-dp/dr max) in the Group Ⅱ were significantly lower than those in the Group Ⅰ and Group Ⅲ during reperfusion. According to the Sunamori's method with which the myocardial ultrastructure can be analysed quantitatively, the most serious injury in the ischemic area was found in Group Ⅲ, then Group Ⅱ and Group Ⅰ; in the non-ischemic area, obvious injury was only found in Group Ⅱ. The results suggested that the cardiac function was obviously suppressed during reperfusion after short period of regional ischemia and that the oxygen free radicals might play an important role in this reperfusion injury. The features of myocardial ultrastructure indicated that ultrastructural damage implicated not only ischemic area but also non-ischemic area during reperfusion. was obviously suppressed during reperfusion after short period of regional ischemia and that the oxygen free radicals might play an important role in this reperfusion injury. The features of myocardial ultrastructure indicated that ultrastructural damage implicated not only ischemic area but also non-ischemic area during reperfusion.

Objective To detect the gene expressions of phosphatase and tensin homolog on chromosome ten (PTEN) engineered mesenchymal stem cells (MSCs) and observe their effects on DBTRG glioma cells.Methods Primary culture of human umbilical cord MSCs was performed;48 h after PTEN transfection into MSCs by liposomes,transfection results were detected under microscope.(1) Transfected MSCsPTEN were used as experimental group and MSCs as control group.PTEN protein and gene expressions of the cells from the two groups were detected by Western blotting and real time-PCR;soluble PTEN protein in the culture supematants was measured using ELISA.(2) In vitro cultured DBTRG cells were divided into four groups,and MSCs supernatant and 25％,50％ and 100％ MSCsPTEN supernatants were added into the four groups,respectively;24 h after culture,calcein AM/EthD-1 staining was used to detect the activity of DBTRG cells which co-cultured with different percentages of MSCsPTEN medium.(3) In vitro cultured DBTRG cells were divided into three groups,and MSCs supernatant and 25％ and 100％ MSCsPTEN supernatants were added into the three groups;RTCA was used to observe the growth curve of DBTRG cells.Results (1) A large number of red fluorescence masses were noted in the MSCsPTEN cells by microscope;real time-PCR and Western blotting indicated that the gene and protein expressions of PTEN in the experimental group were significantly higher than those in the control group (P＜0.05).PTEN content in the supernatants of the experimental group was significantly higher than that in the control group (P＜0.05).(2) CalceinAM/EthD-1 staining indicated that 25％,50％ and 100％ MSCsPTEN supernatant groups had significantly larger number of death DBTRG cells than MSCs supernatant group (P＜0.05);and with the increase of MSCsPTEN supeenatant percentages,the number of death DBTRG cells became larger (P＜0.05).(3) RTCA indicated that as compared with the MSCs supernatant group,25％ and 100％ MSCsPTEN supernatant groups had decreased DBTRG cell index.Conclusion After MSCsPTEN transfection,MSCsPTEN cells can stablely express targeted gene,and their supernatant can obviously promote the death of DBTRG cells and inhibit the growth of glioma cells;PTEN engineered MSCs may be an effective gene therapy for gliomas.