足细胞分子nephrin在高血压大鼠肾脏的表达及作用

The expression and role of nephrin at the podocytes in the kidney of the spontaneously hypertensive rats

目的探讨足细胞分子nephrin在自发性高血压大鼠（SHR）肾脏的表达及作用。方法监测不同时期SHR与京都大鼠（wistar-kyotorats，WKY）尾动脉收缩压（SBP）、尿β2-微球蛋白（β2-MG）、尿素氮（BUN）、血肌酐（SCr）水平；免疫组化、RT-PCR方法检测nephrin蛋白及mRNA的表达，观察肾脏的病理改变。结果与WKY组相比，SHR组SBP、β2-MG、BUN、SCr升高，nephrin蛋白及mRNA表达量下降，且nephrin含量与尿β2-MG呈负相关。SHR组肾脏发生病理改变。结论足细胞分子nephrin在SHR肾小球表达减少，可能是导致足细胞裂隙膜损伤，引起尿β2-MG排泄水平增加，肾功能受损，肾脏病理改变的基础。

Objective To study the changes and the role of the key podocyte molecule nephrin in spontaneously hypertensive rats （SHR）. Methods The systolic blood pressure （SBP） of rat tail artery, urinary β2-microglobulin （β2-MG）,blood urea nitrogen （BUN）, and creatinine （SCr） levels of and were monitored at different stages. The expression of nephrin in the kidney was detected by using immunohistochemical and RT-PCR methods. The pathological changes of the kidney were observed under the microscopy. Results The SBP, β2-MG, BUN, and SCr in SHR group were significantly higher, while the expression of nephrin was lower than in WKY group. The image analysis suggested that the positive area of nephrin was reduced in SHR group as compared with WKY group, and it was negative- ly correlated with the urinary β2-MG. Conclusions The reduction of the expression of the podocyte molecule nephrin in glomerulus of the SHR may lead to injury of fracture membrane at the podoeytes, causing the increase in the excretion of urinary β2-MG, and impairing renal function.