CAJ | 학술논문

目的：探讨睾酮受体（ AR）在高血压肾脏损害中的作用并初步探讨其机制。方法：30只大鼠分为对照组、假手术组和模型组，每组10只；模型组以“两肾一夹法”建立肾血管性高血压大鼠模型。采用免疫组化法检测大鼠肾组织AR和丝裂素活化蛋白激酶磷酸酶1（ MKP-1）蛋白的表达。结果：与对照组相比，模型组大鼠肾组织AR与MKP-1蛋白的表达水平降低（F＝31．043、51．681，P＜0．001）；相关分析发现，模型组大鼠肾组织中AR蛋白与MKP-1蛋白的表达呈正相关（r＝0．744，P＝0．014）。结论：AR蛋白可能参与了高血压肾脏损害的过程，其机制可能与AR和MKP-1信号转导通路偶联有关。
목적：탐토고동수체（ AR）재고혈압신장손해중적작용병초보탐토기궤제。방법：30지대서분위대조조、가수술조화모형조，매조10지；모형조이“량신일협법”건립신혈관성고혈압대서모형。채용면역조화법검측대서신조직AR화사렬소활화단백격매린산매1（ MKP-1）단백적표체。결과：여대조조상비，모형조대서신조직AR여MKP-1단백적표체수평강저（F＝31．043、51．681，P＜0．001）；상관분석발현，모형조대서신조직중AR단백여MKP-1단백적표체정정상관（r＝0．744，P＝0．014）。결론：AR단백가능삼여료고혈압신장손해적과정，기궤제가능여AR화MKP-1신호전도통로우련유관。
Aim:To explore the role of androgen receptor ( AR) in injury of hypertensive kidney and explore the mech-anism.Methods:Thirty rats were allocated into 3 groups:control group , sham operation group and model group , with 10 rats in each group;the rats in model group were made renovascular hypertension model .The expressions of AR and mito-gen-activated protein kinase phosphatase-1 ( MKP-1 ) were detected by immunohistochemistry .Results: In contrast with control group, the protein expression levels of AR and MKP-1 in model group were significantly reduced ( F=31.043, 51.681,P<0.001).Linear correlation analysis showed there was positive correlation between the expression level of AR protein and that of MKP-1 protein in the model group(r=0.744,P=0.014).Conclusion:AR may participate in the hy-pertensive renal injury ,which may be explained by MKP-1 signaling pathway that couples with AR .