硒是健康必需的微量元素,只能通过食物获得。然而,牛硒缺乏的病理过程很少受到关注。这项研究调查了硒缺乏对氧化应激的影响,凋亡,炎症,与健康的小牛作为对照相比,断奶小牛的肺坏死。与对照组相比,缺硒小牛的肺硒含量和11种硒蛋白mRNA的表达显着降低。病理结果显示肺泡毛细血管充盈,增厚的肺泡间隔,整个肺泡隔弥漫性间质炎症。GSH和T-AOC的水平,以及CAT,SOD,和TrxR活动,与健康小牛相比显著下降。MDA和H2O2显著升高。同时,Se-D组的细胞凋亡激活被验证。接下来,在Se-D组中,几种促炎细胞因子表达较高。进一步的研究表明,Se-D组的肺经历了通过过度活跃的NF-κB和MAPK途径的炎症。c-FLIP的高水平表达,MLKL,RIPK1和RIPK3表明坏死性凋亡在硒缺乏期间也会引起肺损伤。
Selenium is an essential trace element for health that can only be obtained through food. However, the pathological processes of selenium deficiency in cattle have received little attention. This study investigated the effects of selenium deficiency on oxidative stress, apoptosis, inflammation, and necroptosis in the lungs of weaning calves compared with healthy calves as controls. The lung selenium content and the expression of 11 selenoproteins mRNA in selenium-deficient calves were substantially reduced compared with the controls. Pathological results showed engorged alveolar capillaries, thickened alveolar septa, and diffuse interstitial inflammation throughout the alveolar septa. The levels of GSH and T-AOC, as well as the CAT, SOD, and TrxR activities, were significantly decreased compared with healthy calves. MDA and H2O2 were significantly elevated. Meanwhile, the apoptosis activation in the Se-D group was validated. Next, in the Se-D group, several pro-inflammatory cytokines showed higher expression. Further research revealed that the lungs in the Se-D group experienced inflammation via hyperactive NF-κB and MAPK pathways. The high level of expression of c-FLIP, MLKL, RIPK1, and RIPK3 indicated that necroptosis also causes lung damage during selenium deficiency.