Department of Physiology, Hebei University of Chinese Medicine, Shijiazhuang 050200, Hebei, China.
Scientific Research Center, Hebei University of Chinese Medicine, Shijiazhuang 050200, Hebei, China.
Molecules. 2019 Mar 26;24(6):1184. doi: 10.3390/molecules24061184.
Iron-induced oxidative stress has been found to be a central player in the pathogenesis of kidney injury. Recent studies have indicated H₂ can be used as a novel antioxidant to protect cells. The present study was designed to investigate the protective effects of H₂ against chronic intermittent hypoxia (CIH)-induced renal injury and its correlation mechanism involved in iron metabolism. We found that CIH-induced renal iron overloaded along with increased apoptosis and oxidative stress. Iron accumulates mainly occurred in the proximal tubule epithelial cells of rats as showed by Perl's stain. Moreover, we found that CIH could promote renal transferrin receptor and divalent metal transporter-1 expression, inhibit ceruloplasmin expression. Renal injury, apoptosis and oxidative stress induced by CIH were strikingly attenuated in H₂ treated rats. In conclusion, hydrogen may attenuate CIH-induced renal injury at least partially via inhibiting renal iron overload.
铁诱导的氧化应激已被发现是肾脏损伤发病机制中的一个核心因素。最近的研究表明，氢气可以作为一种新型抗氧化剂来保护细胞。本研究旨在探讨氢气对慢性间歇性低氧（CIH）诱导的肾损伤的保护作用及其与铁代谢相关的机制。我们发现，CIH 可导致肾脏铁过载，同时伴有细胞凋亡和氧化应激增加。Perl 染色显示，铁主要蓄积在大鼠的近端肾小管上皮细胞中。此外，我们发现 CIH 可促进肾脏转铁蛋白受体和二价金属转运蛋白 1 的表达，抑制铜蓝蛋白的表达。氢气处理可显著减轻 CIH 诱导的大鼠肾脏损伤、细胞凋亡和氧化应激。综上所述，氢气可能通过抑制肾脏铁过载来减轻 CIH 诱导的肾脏损伤。
