尾加压素 Ⅱ 受体拮抗剂 (urantide) 减轻动脉粥样硬化大鼠肾脏损伤.

Objective To explore the mechanism of action of urantide in ameliorating renal injury caused by atherosclerosis (AS). Methods The rats were divided into normal group, model group which were treated with ip VitD3 150 U/(kg·d-1) for 3 consecutive days, and fed with high-fat special diet, with an experimental period of 6 weeks], simvastatin group [5 μg/(kg·d-1) for 14 consecutive days] and intervention model group [urantide 30 μg/(kg·d-1), 7 d and 14 d]. Microscopy was performed for observing pathological changes in the kidney and evaluation of the degree of renal tissue damage. RT-qPCR and immuno-histochemical staining microscopy was used to detect the expression of related genes and proteins. Results Compared to the normal group, the model group showed glomerular atrophy in the renal tissue and adhesion with surrounding tissues. The experiment found a series of changes in renal tubular epithelial cells, such as edema and degeneration, accompanied by a small area of cell necrosis. Sclerosis was found in the glomerulus; Increased positive expression of genes and proteins related to JAK2 and STAT3 (P＜0.05,P＜0.01) was found. Compared to the model group, urantide groups with prolongated medicine administration and the pathological changes that occur in the kidney tissue showed obvious improvement and upturned. At the same time, the degree of glomerulosclerosis decreased and renal tubulointerstitial injury was improved (P＜0.01) ; Positive expression of genes and proteins related to JAK2 and STAT3 (P＜0.05, P＜0.01) all decreased. Conclusions Urantide may inhibit JAK2/STAT3 signal pathway and this finding may support the development of clinical strategy for the prevention and treatment of AS related renal injury. [ABSTRACT FROM AUTHOR]