Elmezzi Graduate School of Molecular Medicine, Manhasset, New York; The Center for Immunology and Inflammation, Feinstein Institute for Medical Research, North Shore-LIJ Health System, Manhasset, New York; and.
The Center for Immunology and Inflammation, Feinstein Institute for Medical Research, North Shore-LIJ Health System, Manhasset, New York; and.
Am J Physiol Renal Physiol. 2014 Aug 15;307(4):F369-84. doi: 10.1152/ajprenal.00127.2014. Epub 2014 Jun 18.
Despite its success as a potent antineoplastic agent, ∼25% of patients receiving cisplatin experience acute kidney injury (AKI) and must discontinue therapy. Impaired magnesium homeostasis has been linked to cisplatin-mediated AKI, and because magnesium deficiency is widespread, we examined the effect of magnesium deficiency and replacement on cisplatin-induced AKI in physiologically relevant older female mice. Magnesium deficiency significantly increased cisplatin-associated weight loss and markers of renal damage (plasma blood urea nitrogen and creatinine), histological changes, inflammation, and renal cell apoptosis and modulated signaling pathways (e.g., ERK1/2, p53, and STAT3). Conversely, these damaging effects were reversed by magnesium. Magnesium deficiency alone significantly induced basal and cisplatin-mediated oxidative stress, whereas magnesium replacement attenuated these effects. Similar results were observed using cisplatin-treated LLC-PK1 renal epithelial cells exposed to various magnesium concentrations. Magnesium deficiency significantly amplified renal platinum accumulation, whereas magnesium replacement blocked the augmented platinum accumulation after magnesium deficiency. Increased renal platinum accumulation during magnesium deficiency was accompanied by reduced renal efflux transporter expression, which was reversed by magnesium replacement. These findings demonstrate the role of magnesium in regulating cisplatin-induced AKI by enhancing oxidative stress and thus promoting cisplatin-mediated damage. Additional in vitro experiments using ovarian, breast, and lung cancer cell lines showed that magnesium supplementation did not compromise cisplatin's chemotherapeutic efficacy. Finally, because no consistently successful therapy to prevent or treat cisplatin-mediated AKI is available for humans, these results support developing more conservative magnesium replacement guidelines for reducing cisplatin-induced AKI in cancer patients at risk for magnesium deficiency.
尽管顺铂作为一种有效的抗肿瘤药物取得了成功,但仍有约 25%的接受顺铂治疗的患者会出现急性肾损伤(AKI),并必须停止治疗。镁稳态的破坏与顺铂介导的 AKI 有关,而且由于镁缺乏很普遍,我们研究了镁缺乏和补充对生理相关的老年雌性小鼠顺铂诱导 AKI 的影响。镁缺乏显著增加了顺铂相关的体重减轻和肾功能损伤标志物(血浆血尿素氮和肌酐)、组织学变化、炎症和肾小管细胞凋亡,并调节了信号通路(如 ERK1/2、p53 和 STAT3)。相反,镁可以逆转这些损伤作用。单独的镁缺乏显著诱导了基础和顺铂介导的氧化应激,而镁补充则减弱了这些作用。在暴露于不同镁浓度的用顺铂处理的 LLC-PK1 肾上皮细胞中也观察到了类似的结果。镁缺乏显著增加了肾脏中的铂蓄积,而镁补充则阻止了镁缺乏后的铂蓄积增加。在镁缺乏期间,肾脏中的铂蓄积增加伴随着肾脏外排转运体表达的减少,而镁补充则逆转了这一现象。这些发现表明,镁通过增强氧化应激从而促进顺铂介导的损伤,在调节顺铂诱导的 AKI 中发挥作用。使用卵巢癌、乳腺癌和肺癌癌细胞系进行的额外体外实验表明,镁补充不会影响顺铂的化疗疗效。最后,由于目前尚无针对人类预防或治疗顺铂介导的 AKI 的有效治疗方法,这些结果支持制定更保守的镁补充指南,以减少有镁缺乏风险的癌症患者的顺铂诱导的 AKI。