伊诺斯
骨化三醇
肾
内分泌学
内科学
内皮素受体
肾脏疾病
医学
骨化三醇受体
肌酐
一氧化氮合酶
受体
一氧化氮
维生素D与神经学
作者
Eryna Ayu Nugra Desita,Nur Arfian,Wiwit Ananda Wahyu Setyaningsih,Dwi Cahyani Ratna Sari
标识
DOI:10.1139/cjpp-2022-0130
摘要
Kidney ischemia–reperfusion injury (IRI) causes acute kidney injury with increasing risk of maladaptive repair through endothelin-1 (ET-1)/endothelin type A receptor (ET A R) signaling. Calcitriol shows renoprotection in kidney fibrosis, however, its effects on vasoactive substances expression and vascular remodeling following kidney IRI remain unclear. This research aimed to investigate Calcitriol’s effects on preproendothelin-1 ( ppET-1), ET A R, endothelial nitric oxide synthase ( eNOS) mRNA expression and vascular remodeling in acute and chronic phases of kidney IRI in mice. Twenty-five male Swiss mice were randomly divided into five groups ( n = 5): SO (sham-operated), IR3 (3 day kidney IRI), IR12 (12 day kidney IRI), IRD3 (3 day kidney IRI + Calcitriol 0.5 µg/kg body weight (BW)/day), and IRD12 (12 day kidney IRI + Calcitriol 0.5 µg/kg BW/day). Ischemia–reperfusion injury groups underwent bilateral renal pedicles clamping for 30 min, then reperfusion. Kidneys were harvested for Sirius Red staining to observe interstitial fibrosis and vascular remodeling, polymerase chain reaction to quantify ppET-1, endothelin type B receptor ( ET B R), eNOS mRNA expression, and Western blotting to quantify ET A R protein expression. Calcitriol treatment in both phases of kidney IRI showed lower serum creatinine and ET A R protein expression, while higher eNOS and ET B R mRNA expression than IRI-only groups. Furthermore, ppET-1 mRNA expression was higher in IRD3 than IR3, but lower in IRD12 than IR12. Calcitriol also prevented vascular remodeling as indicated by lower wall thickness and higher lumen/wall area ratio than IRI-only groups.
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