Zinc (Zn) is a trace element with a variety of anti-inflammatory and antioxidant effects. Zn deficiency is related to tissue fibrosis. The present study was designed to investigate the effect of Zn on renal fibrosis. Mouse models were successfully established by feeding mice diets with different concentrations of Zn. Zn deficiency induced a decrease in Zn levels in kidney tissue. The results also revealed renal vasodilation, hyperemia, and inflammatory cell infiltration, and the levels of creatinine and urea nitrogen were increased. Furthermore, the TUNEL results showed a large degree of renal cell necrosis caused by Zn deficiency. Meanwhile, the corresponding antioxidant and anti-inflammatory regulators (MT-1, MT-2, Nrf2, and TGF-β1) were detected by RT-PCR, showing that the expression of MT-1, MT-2, and Nrf2 decreased but that TGF-β1 expression increased. The results of Sirius red staining proved that the expression of collagen was increased by Zn deficiency. The immunohistochemical experiments found that the expression of α-smooth muscle actin (α-SMA) increased. ELISA showed that the expression of Collagen I, III, and IV; fibronectin (FN); and inflammatory factors (TNF-α and IL-1β) were remarkably increased. The expression of MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, MMP-12, and TIMP-1, which are extracellular matrix-regulating molecules, was detected by RT-PCR. The results showed that the expression of TIMPs was increased but that the expression of MMPs was decreased. We also obtained consistent results in vivo. All the experimental results indicated that Zn deficiency could aggravate fibrosis by increasing inflammation in the kidney.

中文翻译：

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缺锌加剧 ROS 和炎症性损伤导致小鼠肾纤维化。

锌（Zn）是一种具有多种抗炎和抗氧化作用的微量元素。缺锌与组织纤维化有关。本研究旨在研究锌对肾纤维化的影响。通过给小鼠喂食不同浓度的锌，成功建立了小鼠模型。缺锌会导致肾组织中锌含量降低。结果还显示肾血管扩张、充血和炎症细胞浸润，肌酐和尿素氮水平升高。此外，TUNEL 结果显示缺锌引起的肾细胞坏死程度较大。同时通过RT-PCR检测相应的抗氧化和抗炎调节因子（MT-1、MT-2、Nrf2和TGF-β1），表明MT-1、MT-2、和 Nrf2 减少但 TGF-β1 表达增加。天狼星红染色结果证明缺锌会增加胶原蛋白的表达。免疫组化实验发现α-平滑肌肌动蛋白（α-SMA）表达增加。ELISA显示Collagen I、III、IV的表达；纤连蛋白 (FN); 和炎症因子（TNF-α和IL-1β）显着增加。通过RT-PCR检测细胞外基质调节分子MMP-1、MMP-2、MMP-3、MMP-7、MMP-9、MMP-12和TIMP-1的表达。结果表明，TIMPs的表达增加，而MMPs的表达减少。我们还在体内获得了一致的结果。所有的实验结果都表明，缺锌会通过增加肾脏炎症来加重纤维化。天狼星红染色结果证明缺锌会增加胶原蛋白的表达。免疫组化实验发现α-平滑肌肌动蛋白（α-SMA）表达增加。ELISA显示Collagen I、III、IV的表达；纤连蛋白 (FN); 和炎症因子（TNF-α和IL-1β）显着增加。通过RT-PCR检测细胞外基质调节分子MMP-1、MMP-2、MMP-3、MMP-7、MMP-9、MMP-12和TIMP-1的表达。结果表明，TIMPs的表达增加，而MMPs的表达减少。我们还在体内获得了一致的结果。所有的实验结果都表明，缺锌会通过增加肾脏炎症来加重纤维化。天狼星红染色结果证明缺锌会增加胶原蛋白的表达。免疫组化实验发现α-平滑肌肌动蛋白（α-SMA）表达增加。ELISA显示Collagen I、III、IV的表达；纤连蛋白 (FN); 和炎症因子（TNF-α和IL-1β）显着增加。通过RT-PCR检测细胞外基质调节分子MMP-1、MMP-2、MMP-3、MMP-7、MMP-9、MMP-12和TIMP-1的表达。结果表明，TIMPs的表达增加，而MMPs的表达减少。我们还在体内获得了一致的结果。所有的实验结果都表明，缺锌会通过增加肾脏炎症来加重纤维化。