Mechanism Of Exhausted Training Induced Chronic Kidney Injury And The Protective Effects Of EPO On ETICKI In Rats

Objects:The aims of present study were to investigate the protective effects and the mechanisms of Erythropoietin on the chronic kidney damage following 4 weeks exhausted movement in rats.Methods:chronic renal damage model was established with 4 weeks exhaustion movement in rats, rhEPO intervened with this model. HE dying of histopathological changes of renal was detected with Optical microscope; electron microscopy examined pulp ultra structure of renal in rats; TUNEL tested renal cell apoptosis, testing rat serum urea nitrogen, MDA and SOD, NO, NOS, Hb content, RBC counting, urine protein content; with immunohistochemical, fluorescent marker and West-blot testing kidney tissues EPO EPOR, Caspase-3/ and Bcl-XL, NF-?B, TGF-B1, a-SMA, Akt JAK2, the protein expression.Results:1. After repeated 4 weeks exhaustion movement, compared with normal control group, the weight, ran distance, serum Hb in rats declined significantly (P<0.05), serum BUN, urinary protein content increased significantly (P<0.05), kidney organization structure and ultra structural obvious pathological changed.2. After repeated 4 weeks exhaustion movement, compared with control group, the EPOR and EPO protein expression increased significantly in chronic renal injury (P< 0.05).3. General condition improved obviously in exhausted rats after appling for rhEPO, extended running miles,compared with control, BUN,Hb and urine protein are obvious reduced (P< 0.05), the apoptotic cells of kidney tissues significantly reduced(P<0.05), kidney tissues ultra structure, pathological damage improved obviously.4. Compared with normal control groups, rhEPO can obviously increases NO,NOS activity and Bcl-xl, JAK2, Akt protein expression (P< 0.05), significant antagonists inflammatory nuclear factor NF-KB, fibrosis factors-1, a-SMA, Caspase-3 express (P< 0.05).Conclusion:1. Repeated 4 weeks exhaustion movement can cause chronic renal injury in rats.2. The model of chronic kidney damage, kidney tissues EPOR/EPOR protein expression increases, hinting endogenous EPOR/EPOR in chronic renal damage/the intrinsic repair mechanisms.3. rhEPO can reduce chronic renal tissue injury induced by exhausted movement in rats and improve the morphological and renal function, obviously improving the sports ability. rhEPO has antioxidant stress response, elevates nitric oxide (NO), NOS activity, antagonists NF-?B, TGF, a-SMA expression and (or) reduces renal tissue cell apoptosis and reduces chronic renal injury.4. rhEPO can significantly reduce chronic renal injury, may increase Bcl-XL expression, reduce Caspase-3 expression and play the role of antiapoptotic. In this model, EPO/EPOR may pass PI3K/Akt signal transduction pathways playing a protective role.