CAJ | 학술논문

目的：研究C-型利钠肽（CNP）/B-型利钠肽受体（NPR-B）效应轴与C-型利钠肽受体（NPR-C）/中性肽链内切酶（NEP）清除途径在单侧输尿管梗阻（UUO）大鼠肾脏的表达情况。方法原位杂交、荧光定量PCR、免疫组化和Western blot检测UUO大鼠术后24 h、72 h、1周、2周、3周、1个月、2个月和3个月时肾脏CNP、NPR-B、NPR-C、NEP及IV型胶原mRNA和蛋白的表达情况。结果 CNP主要表达于肾小管上皮细胞，在梗阻后即刻显著增加，随疾病进展增幅逐渐衰减。CNP高表达主要归因于UUO早期NPR-B表达上调。结论 NEP和NPR参与肾小管间质纤维化病程中CNP表达调控；NPR-C和NEP表达渐增是导致CNP增幅降低的可能原因。
목적：연구C-형리납태（CNP）/B-형리납태수체（NPR-B）효응축여C-형리납태수체（NPR-C）/중성태련내절매（NEP）청제도경재단측수뇨관경조（UUO）대서신장적표체정황。방법원위잡교、형광정량PCR、면역조화화Western blot검측UUO대서술후24 h、72 h、1주、2주、3주、1개월、2개월화3개월시신장CNP、NPR-B、NPR-C、NEP급IV형효원mRNA화단백적표체정황。결과 CNP주요표체우신소관상피세포，재경조후즉각현저증가，수질병진전증폭축점쇠감。CNP고표체주요귀인우UUO조기NPR-B표체상조。결론 NEP화NPR삼여신소관간질섬유화병정중CNP표체조공；NPR-C화NEP표체점증시도치CNP증폭강저적가능원인。
Objectives To study the expression features of C-type natriuretic peptide (CNP)/natriuretic peptide receptor-B (NPR-B) axis and two parallel elimination pathways, natriuretic peptide receptor-C (NPR-C) and neutral endopeptidase (NEP) in unilateral ureteral obstruction (UUO) rats. Methods CNP, NPR-B, NPR-C, NEP, Col-IV and type IV collagen (Col-IV) mRNA and proteins were determined by in situ hybridization, real-time PCR, immunohistochemistry and western blot in UUO rats at 24h, 72h, 1w, 2w, 3w, 1m, 2m and 3m. Results CNP expression tended to be higher immediately after ligation and de-clined along with the progression of disease, occurring predominantly in tubular epithelial cells. A high-level CNP may attribute to the elevated expression of NPR-B in the early phase of UUO. Conclusions NEP and NPR participate in the regulation of CNP expression in tubulointerstitial fibrosis. The gradual increased expression of NPR-C and NEP may cause the subsequent de-cline of CNP.