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糖尿病肾病患者血清抗AT_1、α_1、β_1和M_2受体自身抗体与肾损害的关系 被引量:6

Relationship of the autoantibodies against AT_1,α_1,β_1,M_2 receptor with renal damage in diabetic nephropathy
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摘要 目的探讨抗血管紧张素Ⅱ受体1型(AT_1受体)、α_1受体、β_1受体、M_2受体自身抗体是否与糖尿病肾病(DN)有关。方法以合成的AT1、β_1、α_1和M_2受体多肽片段为抗原,应用ELISA技术,检测171例DN患者,71例2型糖尿病无肾损害患者(DM组),60例高血压无肾损害(HT)组及41例正常人(NC)血清中抗AT_1、α_1、β_1和M_2受体自身抗体。结果 DN组抗AT_1、α_1、β_1和M_2受体抗体阳性率分别为46.2%、44.4%、53.2%、42.7%,明显高于DM组(12.7%、8.5%、11.3%、7.0%)、HT组(15.0%、11.7%、8.3%、10.0%)及NC组(9.8%、12.1%、7.3%、12.2%)(P均<0.01);DN亚组微量自蛋白尿(早期肾病)和大量白蛋白尿组(临床肾病)受体自身抗体阳性率分析,2组差异有统计学意义(P<0.05)。结论抗G蛋白偶联受体自身抗体不仅与DN有关而且与肾损害程度有关,自身免疫机制参与了DN发病过程。 Objective To explore the role of the autoantibodies against angiotensin Ⅱ type 1 receptor (AT1 receptor), α1 adrenergic receptor (α1 receptor),β1 adrenergic receptor (β1 receptor) and M2-muscarrinic receptor(M2-receptor) in the development of diabetic nephropathy. Methods The epitopes of the second extracellular loop of AT1 receptor (165-191), al receptor (192-218), β1 receptor (197-222) and M2 receptor (169-191) were synthesized and used respectively to screen sera autoantibodies in patients with diabetic nephropathy (DN) (n =171), diabetes mellitus without renal damage (DM) (n = 71), hypertension without renal failure(n=71) and healthy blood donors (n=41, control) by ELISA. Results The positive rates of the autoantibodies against AT1 receptor, α1 receptor,β1 receptor, M2 receptor were higher in DN group (46. 2% ,44. 4%, 53.2%,42. 7%, respectively) than in HT group. (15.0%, 11.7%, 8. 3 % and 10. 0%, respectively, all P〈0. 05), and than in healthy donors (9.8%, 12.1%, 7. 3 % and 12.2%, respectively,all P〈0. 05) ,and than in DM (12.7% ,8. 5% ,11.3%and 7. 0 %, respectively,all P〈0. 05). Conclusions The autoantibodies against AT1-receptor, α1-receptor, β1-receptor, M2-receptor may play important roles in the pathogenesis of diabetic nephropathy.
出处 《中国糖尿病杂志》 CAS CSCD 北大核心 2009年第6期409-411,共3页 Chinese Journal of Diabetes
基金 湖北省自然科学基金项目(2002AB116)
关键词 糖尿病肾病 受体 自身抗体 肾损害 Diabetic nephropathy Receptor Autoantibody Renal damage
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