ABSTRACT
OBJECTIVE: To investigate the expression status and clinical significance of cytoprotective proteins to human renal allografts. METHODS: Expressions of cytoprotective proteins: antiapoptotic protein (A20), hemeoxygenase-1 (HO-1), and B-cell lymphoma/leukemia-X(L) (Bcl-X(L)) were analyzed by immunohistochemistry and compared in 30 renal allografts, including 10 grafts undergoing acute rejection (AR), 10 grafts undergoing chronic rejection (CR), and 10 nonrejecting (NR) grafts. RESULTS: Expressions of A20, HO-1 and Bcl-X(L) localized mainly in endothelial, smooth muscle, and infiltrating mononuclear cells. A20 expressed in grafts undergoing AR (5.04 +/- 0.71) and CR (3.20 +/- 0.64), not in NR grafts, and its expression in CR was weaker than that in AR ( P < 0.01). HO-1 expressed in AR (7.91 +/- 2.24), not in CR and NR. Bcl-X(L) was detected in all grafts (AR: 10.62 +/- 3.17; CR: 8.50 +/- 2.45; NR: 11.03 +/- 2.77), but had a decreased expression levels in CR. CONCLUSION: A20 and HO-1 may play protective role for AR, and A20 may be the essential protein having protective function for CR.
Subject(s)
Heme Oxygenase-1/metabolism , Intracellular Signaling Peptides and Proteins/metabolism , Kidney Transplantation , Nuclear Proteins/metabolism , bcl-X Protein/metabolism , DNA-Binding Proteins , Graft Rejection/metabolism , Humans , Transplantation, Homologous , Tumor Necrosis Factor alpha-Induced Protein 3ABSTRACT
OBJECTIVE: To establish an accelerated animal model of the chronic renal allograft dysfunction in rat. METHODS: Kidney transplantation was performed from SD to Wistar strain (allogeneic) according to the procedure of Kamada with some modification. Before the transplantation, the kidney was preserved in 0-4 degrees C heparin sodium chloride solution for prolonging the one hour. The serum creatinine level and pathological change of transplant kidney were observed in the 2nd, 4th, 6th, 8th and 12th weeks post-transplantation. RESULTS: After transplantation, the serum creatinine level of recipient rats obviously increased in the 6th week and the pathologic changes of chronic nephropathy evidently appeared in the 8th week when compared to those of the control group with non-reinforcement I/R injury; a statistically significant difference was noted. CONCLUSION: It is simple and feasible to establish a rat model of (SD-->Wistar) transplant kidney-sclerosis accelerated by prolonging I/R injury.
