Antagonistic effects of nano-selenium on broilers hepatic injury induced by Cr(VI) poisoning in AMPK pathway
Antagonistic effects of nano-selenium on broilers hepatic injury induced by Cr(VI) poisoning in AMPK pathway
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DOI：
10.1007/s11356-020-08501-0
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发表时间：
2020-07
影响因子：
5.8
通讯作者：
Tianguang Zhang;Yali Zhao;Lei Li;Dongxing Zhou
中科院分区：
文献类型：
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作者：
Tianguang Zhang;Yali Zhao;Lei Li;Dongxing Zhou
铬是肉鸡常用的饲料添加剂之一，具有三价铬和六价铬。六价铬中毒可引起肉鸡肝脏损伤和代谢紊乱。纳米硒可拮抗重金属引起的生物体氧化损伤和代谢紊乱。选用纳米Se对肉鸡体内六价铬中毒进行拮抗作用研究。AMPK(腺苷5，单磷酸激活的蛋白激酶)是一种细胞能量调节因子，在碳水化合物和脂肪代谢中起着关键的调节作用。本研究选择AMPK途径和ACACA/CPT1两个基因，研究纳米硒对肉鸡铬中毒的防治作用及其分子机制。为此，选择1日龄AA(Arbor Acres)肉鸡180只，随机分为6组(n= ，30只)进行试验。按计划饲养35天后，取肝脏进行进一步检查，包括组织病理学检查、差异基因表达分析，并使用RT-qPCR、蛋白质印迹和免疫组织化学(IHC)等相关技术进一步验证mRNA和蛋白质水平。组织病理学检查显示，铬(VI)中毒组的肝细胞损伤较纳米硒组严重。RT-qPCR结果显示，铬(VI)中毒组ACACA基因的相对表达显著增加(P<； )，而CPT1基因的相对表达显著降低(P<； )。在纳米硒添加组，这些结果正好相反。Western印迹结果与RT-qPCR结果一致，均提示纳米Se对铬(VI)具有拮抗作用。通过形态和组织病理学观察，以及AMPK途径中ACACA1和CPT1A3基因的mRNA和蛋白表达水平的测定，证实纳米硒对肉鸡铬中毒有一定的预防和保护作用。此外，纳米硒可通过AMPK途径拮抗铬(VI)对肉鸡碳水化合物和脂肪代谢的不利影响。为今后肉鸡铬中毒的研究提供了新的方法和实验依据。
Cr (chromium, with common valence states of III and VI) is one of the common broiler feed additives. Liver injury and metabolic disorders could be caused by Cr(VI)(hexavalent chromium) poisoning in broilers. Oxidative damage and metabolic disorders of organisms caused by heavy metals could be antagonized by nano-Se (nano-selenium). Nano-Se was chosen to study the antagonism of Cr(VI)poisoning in broilers. AMPK (Adenosine 5,-monophosphate-activated protein kinase) is known as a “cell energy regulator” and plays a key regulatory role in carbohydrate and lipid metabolism. AMPK pathway andACACA/CPT1Atwo genes were selected to study the prevention and treatment of nano-Se on Cr(VI)poisoning in broilers and its molecular mechanism. For this purpose, 180 1-day-old AA (Arbor Acres) broilers were selected and randomly divided into 6 groups (n= 30) for further testing. After feeding as planned for 35 days, the livers of such broilers were taken for further examination including histopathological examination, differential gene expression analysis, and further validation on both mRNA and protein levels using related techniques like RT-qPCR, western blot, and immunohistochemistry (IHC). The histopathological examination suggested that the liver cells of the Cr(VI)poisoning group were more severely injured than the nano-Se addition group. RT-qPCR results showed that the relative expression ofACACAgene in the Cr(VI)poisoning group was significantly increased (P< 0.05), while theCPT1Agene’s expression was significantly decreased (P< 0.01). Those results were reversed in the nano-Se addition group. Western blot results were consistent with RT-qPCR and both suggested antagonism of nano-Se on Cr(VI). Through morphological and histopathological observation, as well as the measurement of the mRNA and protein expression levels ofACACAandCPT1Agenes in AMPK pathway, it was confirmed that nano-Se has certain preventive and protective effects on Cr(VI)poisoning in broiler chickens. Furthermore, the adverse effects of Cr(VI)on carbohydrate and lipid metabolism in broilers can be antagonized by nano-Se through AMPK pathway. A new method and experimental basis were provided to the future study of Cr(VI)poisoning in broilers.