医学
氧化应激
安普克
炎症
碘普罗胺
脂联素
脂联素受体1
内分泌学
内科学
血尿素氮
肾
化学
生物化学
蛋白激酶A
激酶
糖尿病
胰岛素抵抗
放射科
造影剂
作者
Daqian Gu,Yu Shi,Zhengfan Gong,Tianyang Xia,Hongmei Ren,Duofen He,Jian Yang,Yu Han,Chunyu Zeng
标识
DOI:10.1007/s10157-020-01944-2
摘要
Contrast-induced nephropathy (CIN), a complication caused by using contrast medium during diagnostic and interventional procedures, occurs frequently and lacks effective treatment. AdipoRon, the agonist of adiponectin receptors, has been shown to benefit many organs including the kidney. This study aimed to investigate the role of AdipoRon in treating CIN. CIN model was established via infusing iopromide (1.8 g/kg) in Sprague–Dawley (SD) rats; NRK52E cells were treated with iopromide (5–50 μM). Renal function, renal histopathology, levels of lactate dehydrogenase (LDH) release, cell vitality, oxidative stress and inflammatory markers were measured to evaluate the protective effects of AdipoRon. The level of pAMPK/AMPK was determined by western blot. AdipoRon (50 mg/kg) significantly reversed serum creatinine, blood urea nitrogen, creatinine clearance and urinary kidney injury molecule-1 levels induced by iopromide in SD rats. Besides, it decreased the renal injury score and apoptosis of renal cells. AdipoRon also reversed the changes of antioxidant markers, pro-oxidant and inflammatory markers induced by iopromide. Moreover, the in vitro studies showed that AdipoRon decreased LDH release and increased cell vitality in NRK52E cells treated with iopromide. Then, we demonstrated that the protection of AdipoRon was accompanied by augmented AMPK phosphorylation. Both in vivo and in vitro studies demonstrated that compound c, an AMPK inhibitor, reversed the AdipoRon-mediated improvement in the CIN model. Our data indicate that AdipoRon protects against the CIN by suppressing oxidative stress and inflammation via activating the AMPK pathway, showing that AdipoRon might be a potential candidate for the prevention and therapy of CIN.
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