| Objective : To investigate endogenous transforming factor beta-1 (TGFβ1) and its mRNA in renal following ischemia-reperfusion in rat, and the role of it in organ injury induced by ischemia-reperfusion.Methods : Healthy SD rats were divided randomly into 6 group, including: normal control group(sham-operation n=6),ischemia for 45 min(reperfusion0h, n=6),reperfusion2h,4h,12h,24h group(n=6).The rats were only separated dual kidney pedicle and given no champ in normal group. Renal ischemia reperfusion injury models were founded in other five groups, opened abdominal and placed atraumatic vascular champ in dual kidney pedicle for 45 minutes ,followed by reperfusion 2h,4h,12h,24h.The distribution and content changes of TGFβ1 and its mRNA in renal were observed by means of immunohistochemistry and reverse transcription polymerase chain reaction(RT-PCR).Results:TGFβ1mRNA and protein were expressed in normal and injured renal, mainly in renal tubular cell .a small quantity in renal glomerulus. TGFβ1mRNA and protein level increased at 45 minutes after ischemia than normal control and continue to increase at 2 hours(P<0.05). TGFβ1 gene expression markedly increased at 4 hours and reach the peak at 12 hours after reperfusion compared with normal control(P<0.05) It returned to normal level after 24 hours reperfusion.Conclusions:1. The results suggest that gene expression of endogenous transforming factor-β1(both mRNA and protein)appears to be up following the time of injury after ischemia-reperfusion in rat, and reflects damages degree in early inflammation procedure. 2. Endogenous transforming factor-β1 plays an important role both in early inflammation procedure and inlater renal selfrepair after ischemia-reperfusion and protects renal after ischemia-reperfusion injury in rats. 3. Applying exogenous transforming factor-β1 or improve contents of endogenous transforming factor-β1 through gene-transferred technology in early ischemia-reperfusion process may decrease ischemia-reperfusion injury, protect renal. |