Publications (2)5.03 Total impact
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ABSTRACT: To evaluate the effects of chimerism on the mice heart transplanted survival with the bone marrow infusion. Bone marrow cells (BMCs) were obtained from BALB/c mice. These BMCs were injected into the irradiated (2Gy-Co60) C57BL/6 mice through femoral vein. Then Group A mice were treated with Cyclosporine (1mg/kg) for 21days and Group B were not treated with Cyclosporine. Group C were treated as the control group without BMCs infusion. Group D were treated with Cyclosporine (1mg/kg) for 21days pre-hearttransplantation without BMCs infusion. After 21days, the C57BL/6 mice received heart allografts from BALB/c. To determine the degree of chimerism in BMCs infusion recipients, peripheral blood were isolated on day 7, 14, 21. Allografts were harvested 10days after heart transplantation for the histological analysis. (1) Chimerism detected in the peripheral blood of Group A mice on day 7 after BMCs infusion was 6.1±2.5%, on day 14 was 15.4±2.9% and on day 21 was 10.7±2.6%. For the Group B mice on day 7 after BMCs infusion, the chimerism was 2.8±1.1%, on day 14 was 11.2±4.8% and on day 21 was 7.4±3.7%. For the Groups C and D mice, no chimerism was observed. Group A mice had the tendency toward improved level of chimerism than Group B mice. (2) The survival time of Group A (n=6) was 13.0±1.4days which was significantly longer than Group B (n=6) with the survival time was 8.5±1.3days (p<0.001), also longer than the mice in Groups C and D, the survival time of which were 10.0±1.3days (p=0.008) and 9.4±1.1days (p=0.004). There is no significant difference among Groups B, C, and D. (3) The HE staining showed the much more seriously heart rejection in Groups B, C and D than Group A. The chimerism was found in the BMCs infusion groups. Without the CsA treatment combined with chimerism could not protect the transplanted heart. There was no obvious evidence showed that the chimerism alone could improve the survival time of cardiac allografts in mice.
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ABSTRACT: Abnormal lipid metabolism contributes to the pathogenesis of diabetes, but it is uncertain whether it plays a role in the development of diabetic nephropathy (DN). While rapamycin was shown to prevent DN development in streptozotocin (STZ)-induced diabetic rats in our previous studies, it is unknown if it intervenes with lipid metabolism. We divided the rats into four groups: normal control rats, rapamycin-treated normal rats, diabetic rats and rapamycin-treated DN rats. The apoptosis was evaluated by immunohistochemistry. The crude lipid and sphingolipid were extracted from rat renal cortex and analysed by matrix-assisted laser desorption ionization-time of flight mass spectrometry. The expression of the three key enzymes in sphingolipid metabolism including serine palmitoyltransferase, acid sphingomyelinase and sphingomyelin synthase was measured by western blot and immunohistochemistry in rat renal cortex. The level of apoptosis was increased in diabetic rats, and rapamycin treatment reduced apoptosis. STZ treatment significantly increased formation of many sphingolipids species through elevated de novo synthesis. These changes were inhibited by treatment with rapamycin. Accumulation of sphingolipids contributes to STZ-induced diabetes, and the therapeutic effect of rapamycin on diabetic nephropathy is partly through suppression of sphingolipid abnormality.
Hang-hsien, Zhejiang Sheng, China
- School of Medicine