ABSTRACT
Objective To investigate the roles of tumor necrosisfactor-α(TNF-α) and nuclear factor-κB (NF-κB) in cerebral ischemia-reperfusion injury in rats w ith diabetes mel itus. Methods Thirty-six healthy male Sprague-Daw ley rats w ere divided into a euglycemic sham operation group, a euglycemic isc hemia-reperfusion group, and a diabetes ischemia-reperfusion group (n=12 in each group) according to a random number table. A diabetes model w as induced by intraperitoneal injection of streptozotocin, and then a focal cerebral ischemia-reperfusion model w as induced by the suture method. The neurological deficit score was performed at 24 h after reperfusion. 2,3,5 triphenyl tetrazolium staining was used to measure the cerebral infarction area. Western blotting w as used to detect the expression levels of NF-κB and TNF-αon the ischemic sides. Results The neurological function scores w ere 0.00 ±0.00, 2.50 ±1.08, and 3.20 ± 1.03, respectively in the euglycemic sham operation, euglycemic cerebral ischemia-reperfusion and diabetes cerebral ischemia-reperfusion groups, and there w ere significant differences (F=38.015, P<0.001). The neurological deficit scores of the diabetes cerebral ischemia-reperfusion group w ere significantly aggravated compared with the euglycemic cerebral ischemia-reperfusion group (P<0.05). The infarct areas of the euglycemic sham operation, euglycemic cerebral ischemia-reperfusion and diabetes cerebral ischemia-reperfusion groups w ere 0.00% ±0.00%, 33.09% ±5.17%, and 55.45% ±9.29%, respectively, and there w ere significant differences among the groups (F=206.614, P<0.001), in w hich the infarct area in the diabetes cerebral ischemia-reperfusion group w as enlarged significantly compared w ith the euglycemic cerebral ischemia-reperfusion group ( P< 0.05 ). At 24 h after reperfusion, there w ere no significant differences in the expression levels of the cortical NF-κB (F=29.993, P<0.001) and TNF-α(F=28.722, P<0.001) on the ischemic sides in each group, in w hich the expression levels of NF-κB and TNF-αin the diabetes cerebral ischemia-reperfusion group w ere increased significantly compared w ith the euglycemic cerebral ischemia-reperfusion group (al P<0.05). Conclusions Diabetes may aggravate cerebral ischemia reperfusion injury. The upregulated expression of TNF-αand NF-κB may be one of the mechanisms of diabetes aggravating cerebral ischemia-reperfusion injury.
ABSTRACT
BACKGROUND:Umbilical cord mesenchymal stem cels have strong proliferation and differentiation capacities, and can be induced to differentiate into pancreatic β cels, thereby playing a therapeutic effect on diabetes mel itus. OBJECTIVE:To study the therapeutic effects of transplantation of umbilical cord mesenchymal stem cels for treatment of diabetes melitus in rats. METHODS: Thirty male Sprague-Dawley rats were randomly divided into control group (n=6), transplantation group (n=12) and diabetic group (n=12). Rats in the control group were given normal saline injection. Rats in the other two groups were injected with streptozotocin at a dose of 45 mg/kg to establish diabetic models. After modeling, transplantation of umbilical cord mesenchymal stem celsviatail vein was given in the transplantation group. RESULTS AND CONCLUSION:Thirty days after modeling, the fasting blood glucose was maintained at a higher level in comparison with the control group (P 0.05), but in the diabetic group, the fasting blood glucose level was stil higher and the body mass continued to decrease. These findings indicate that the transplantation of umbilical cord mesenchymal stem cels can be effective in the treatment of diabetes melitus in rats.