Abstract:

ABSTRACT     Objectives: To investigate the effect of exogenous EPO intervention on AKI repair by bone marrow mesenchymal stem cells(BM-MSCs) transplantation, and the role of SDF-1/CXCR4 axle in the effect has also been discussed. Methodology: Altogether one hundred C57BL/6 mice had been randomly divided into five groups. They were normal group (n=20), model group (AKI group, n=20), BM-MSCs transplantation group (n=20), EPO intervention group (n=20), and EPO intervention + BM-MSCs transplantation group (n=20). Transplanted BM-MSCs were marked by BrdU. Some mice had been sacrificed after the model been constructed 1d, 3d, 7d, and 14d respectively; arterial blood was reserved for testing blood BUN and SCr level; pathological changes for renal tissue have been observed and the injury degree for renal tubular has been scored; BM-MSCs distributed in renal tissue for recipient mice were observed with immunohistochemistry method and SDF-1 level in injured renal tissue was tested by Western Blot. Results: Compared with BM-MSCs transplantation group and EPO intervention group, BUN, SCr and ATN scores were declined sharply in EPO internvention + BM-MSCs transplantation group; on the 14th day after the transplantation, BUN, SCr degrees for the mice were even close to that of normal group. IHC showed that BrdU+ cells distribution could be detected in the mice kidneys for BM-MSCs transplantation group, and the value reached to the peak on the 7th day after the surgery （11.3％±1.38％）; EPO intervention combined with BM-MSCs transplantation could increase the number of BrdU+ positive cells in renal tissue. SDF-1 level was raised for renal tissue after AKI model been constructed, which went to the peak on the 7th day after the model been constructed, and SDF-1 expression could be obviously increased with EPO intervention. Conclusions: EPO intervention could increase the number of transplanted cells after BM-MSCs transplantation, enhance AKI repair effect. The high level of SDF-1 expression, which could promote stem cells homing to kidneys, may be one of possible mechanisms. 

Key words: bone marrow mesenchymal stem cells, acute kidney injury, erythropoietin, stromal cell derived factor-1