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Zinc-induced protective effect for testicular ischemia-reperfusion injury by promoting antioxidation via microRNA-101-3p/Nrf2 pathway

机译:锌通过microRNA-101-3p / Nrf2途径促进抗氧化作用对睾丸缺血再灌注损伤的保护作用

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摘要

The present study was performed to determine the protective effect of Zinc on the rat testicular ischemia-reperfusion (I/R) injury and its mechanism. , the pathological changes and the apoptosis index were significantly relieved in the rats with Low-dose Zinc pretreatment, compared to the I/R group. After Low-dose Zinc treatment, the levels of tissue Malondialdehyde (MDA) were significantly decreased, while tissue antioxidant indices were significantly increased. Meanwhile, the level of NF-κB was significantly lower compared to I/R group, while the levels of Nrf2-dependent antioxidant enzymes were significantly higher in Low-dose Zinc+I/R group. , Low-dose Zinc markedly increased Leydig cell (TM3) cell viability, and relieved testicular oxidative damage via down-regulating ROS. A total of 22 differently expressed microRNAs were screened out using microRNA microarray in rat testicular tissue caused by I/R injury, especially showing that miR-101-3p was selected as the target miRNA. Furthermore, the levels of Nrf2 and NF-κB were apparently increased/decreased in TM3 cells treated with Hypoxic/Reoxygenation (H/R) after miR-101-3p mimics/inhibitor. In addition, H/R-induced testicular oxidative damage was recovered in TM3 administrated with miR-101-3p inhibitor and si-Nrf2. Therefore, this study provided a novel insight for investigating protective effect of Zinc on testicular I/R injury by promoting antioxidation via miR-101-3p/Nrf2.
机译:本研究旨在确定锌对大鼠睾丸缺血再灌注(I / R)损伤的保护作用及其机制。与I / R组相比,低剂量锌预处理的大鼠的病理学改变和细胞凋亡指数得到了明显缓解。低剂量锌处理后,组织丙二醛(MDA)的水平显着降低,而组织抗氧化指数显着提高。同时,低剂量锌+ I / R组的NF-κB水平明显低于I / R组,而Nrf2依赖性抗氧化酶的水平明显高于I / R组。低剂量锌通过下调ROS显着增加Leydig细胞(TM3)细胞的活力,并减轻睾丸氧化损伤。使用microRNA微阵列在由I / R损伤引起的大鼠睾丸组织中筛选出总共22种不同表达的microRNA,尤其表明miR-101-3p被选为靶标miRNA。此外,miR-101-3p模拟物/抑制剂后,在低氧/复氧(H / R)处理的TM3细胞中,Nrf2和NF-κB的水平明显升高/降低。另外,在miR-101-3p抑制剂和si-Nrf2给药的TM3中,H / R诱导的睾丸氧化损伤得以恢复。因此,本研究为通过miR-101-3p / Nrf2促进抗氧化作用研究锌对睾丸I / R损伤的保护作用提供了新的见解。

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