Contrast-induced acute kidney injury (CI-AKI) is the third most common cause of hospital-acquired renal failure, with an incidence of 11%. However, the disease mechanism remains unclear, and no effective treatment is available. Paricalcitol has been reported to be effective in animal models of kidney injury. We hypothesized that paricalcitol could play a renoprotective role against CI-AKI. Rats were divided into control, paricalcitol, contrast, and paricalcitol-plus-contrast groups. We used a previously published protocol to produce CI-AKI. Paricalcitol (0.3 μg/kg) was administered intraperitoneally before 24 h and 30 min before indomethacin. We used HK-2 cells to evaluate the effects of paricalcitol on mitophagy and senescence. Ioversol triggered renal dysfunction, increasing blood urea nitrogen and serum creatinine. Significant tubular damage, increased 8-OHdG expression, and apoptosis were apparent. Ioversol injection induced high expression levels of the mitophagy markers Pink1, Parkin, and LC3 and the senescence markers β-galactosidase and p16INK4A. Paricalcitol pretreatment prevented renal dysfunction and reduced tissue damage by reducing both mitophagy and senescence. Cellular morphological changes were found, and expression of LC3B and HMGB1 was increased by ioversol in HK-2 cells. Paricalcitol countered these effects. This study showed that mitochondria might drive injury phenotypes in CI-AKI, and that paricalcitol protects against CI-AKI by decreasing mitochondrial damage.

中文翻译：

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Paricalcitol通过调节线粒体吞噬和衰老来减轻造影剂引起的急性肾脏损伤。

造影剂诱发的急性肾损伤（CI-AKI）是医院获得性肾衰竭的第三大最常见原因，其发生率为11％。然而，该疾病的机制仍不清楚，并且没有有效的治疗方法。据报道帕立骨化醇在肾损伤的动物模型中有效。我们假设paricalcitol可能对CI-AKI起到肾脏保护作用。将大鼠分为对照组，paricalcitol组，对比组和paricalcitol加造影剂组。我们使用以前发布的协议来生产CI-AKI。Paricalcitol（  0.3μ（g / kg）在消炎痛前24小时和30分钟前腹膜内给药。我们使用HK-2细胞评估paricalcitol对线粒体和衰老的影响。Ioversol引发肾功能不全，增加血液尿素氮和血清肌酐。明显的肾小管损害，增加的8-OHdG表达和凋亡。Ioversol注射诱导线粒体标记物Pink1，Parkin和LC3以及衰老标记物β的高表达水平-半乳糖苷酶和p16INK4A。Paricalcitol预处理可通过减少线粒体吞噬和衰老来预防肾功能不全并减少组织损伤。发现细胞形态变化，并通过碘夫醇增加了HK-2细胞中LC3B和HMGB1的表达。Paricalcitol抵抗了这些影响。这项研究表明，线粒体可能会驱动CI-AKI的损伤表型，而帕立骨化醇可以通过减少线粒体的损​​伤来防止CI-AKI。