Li Xiaoran, Lu Jianzhong, Shang Panfeng, Bao Junsheng, Yue Zhongjin
Department of Urology, Gansu Nephro-Urological Clinical Center, Institute of Urology, The Second Hospital of Lanzhou University, 82 Cui Ying Men, Lanzhou, 730030, Gansu, People's Republic of China.
Mol Cell Biochem. 2015 Jan;399(1-2):167-78. doi: 10.1007/s11010-014-2243-8. Epub 2014 Oct 16.
The objective of this study is to examine the effects of apocynin on melamine-cyanuric acid mixture (MCM)-induced nephrolithiasis in vitro and in vivo. For the in vitro experiments, changes in oxidative stress (OS) markers and the expression of osteopontin (OPN) and phospho-p38 (p-p38) were measured to assess the effects of apocynin treatment after MCM-induced crystallization in HK-2 cells, a human renal epithelial-derived cell line. For in vivo studies, the potential effects of apocynin in preventing and treating nephrolithiasis were analyzed with a MCM-induced nephrolithiasis rat model, and urea and creatinine levels were measured. Urinary 8-IP (a product of lipid peroxidation) and malondialdehyde levels and superoxide dismutase activity were assessed in the kidneys as markers of renal OS. The kidneys were removed, weighed, and subjected to histopathological examination. The urolithiasis-associated proteins p-p38 and OPN were evaluated by immunohistochemistry and Western blotting. Apocynin treatment prevented the MCM-induced changes in OS and in OPN and p-p38 expression in HK-2 cells. For in vivo experiments, the expression of OS markers, renal OPN, and p-p38 increased after MCM administration, and these increases were diminished by apocynin. In addition, apocynin prevented MCM-induced renal crystallization. Moreover, prophylactic apocynin treatment reduced MCM-induced nephrotoxicity. After therapeutic apocynin treatment in nephrolithic rats, OS decreased, but the other indicators did not improve significantly. Prophylactic apocynin administration reduced renal melamine-related-crystal deposition, potentially by modulating OS and thereby decreasing p-p38 and OPN expression.
本研究的目的是在体外和体内研究阿扑辛对三聚氰胺 - 氰尿酸混合物(MCM)诱导的肾结石形成的影响。在体外实验中,通过测量氧化应激(OS)标志物、骨桥蛋白(OPN)和磷酸化p38(p - p38)的表达变化,来评估阿扑辛处理对MCM诱导人肾上皮来源细胞系HK - 2细胞结晶后的影响。在体内研究中,利用MCM诱导的肾结石大鼠模型分析阿扑辛预防和治疗肾结石的潜在作用,并测量尿素和肌酐水平。评估肾脏中尿8 - IP(脂质过氧化产物)、丙二醛水平和超氧化物歧化酶活性,作为肾脏OS的标志物。取出肾脏,称重,并进行组织病理学检查。通过免疫组织化学和蛋白质印迹法评估与尿石症相关的蛋白质p - p38和OPN。阿扑辛处理可预防MCM诱导的HK - 2细胞中OS以及OPN和p - p38表达的变化。在体内实验中,MCM给药后OS标志物、肾OPN和p - p38的表达增加,而阿扑辛可减轻这些增加。此外,阿扑辛可预防MCM诱导的肾脏结晶。而且,预防性给予阿扑辛可降低MCM诱导的肾毒性。在肾结石大鼠中进行治疗性阿扑辛处理后,OS降低,但其他指标未显著改善。预防性给予阿扑辛可减少肾脏中与三聚氰胺相关的晶体沉积,可能是通过调节OS从而降低p - p38和OPN的表达。