Abstract：
Selenium deficiency can lead to multiple tissue and organ damage in the body and could coexist with chronic toxic exposures. Contamination from Bisphenol A (BPA) exposure can induce the occurrence of various injuries including pyroptosis. However, it is not clear whether selenium deficiency and BPA exposure affect tracheal tissue pyroptosis in chickens. To investigate whether selenium deficiency and BPA exposure induce chicken tracheal tissue pyroptosis via the NF-κB/NLRP3/Caspase-1 pathway and the effect of their combined exposure on tissue injury, we developed a model of relevant chicken tracheal injury. Sixty broilers were divided into four groups: the control group (C group), selenium-deficient group (SeD group), BPA-exposed group (BPA group) and combined exposure group (SeD + BPA group). The study examined the expression indicators of markers of pyroptosis (NLRP3&GSDMD), NF-κB pathway-related inflammatory factors (NF-κB, iNOS, TNF-α, COX-2), pyroptosis-related factors (ASC, Caspase-1, IL-1β, IL-18), and some heat shock proteins and interleukins (HSP60, HSP90, IL-6, IL-17) in the samples. The results showed that the expression of the above indicators was significantly upregulated in the different treatment groups (P < 0.05). In addition, the expression levels of the above related indicators were more significantly up-regulated in the combined selenium-deficient and BPA-exposed group compared to the group in which they were individually exposed. It was concluded that selenium deficiency and BPA exposure induced tracheal tissue pyroptosis in chickens through NF-κB/NLRP3/Caspase-1 pathway, and BPA exposure exacerbated selenium deficiency-induced tracheal pyroptosis. The present study provides new ideas into studies related to the co-exposure of organismal micronutrient deficiency and chronic toxicants.
摘要：
硒缺乏可导致体内多个组织和器官损伤，并可能与慢性毒性暴露共存。双酚A（BPA）暴露引起的污染可引起各种损伤的发生，包括焦凋亡。然而,尚不清楚硒缺乏和BPA暴露是否会影响鸡的气管组织焦亡。探讨硒缺乏和BPA暴露是否通过NF-κB/NLRP3/Caspase-1通路诱导鸡气管组织焦亡及其联合暴露对组织损伤的影响。我们建立了相关的鸡气管损伤模型。将60只肉鸡分为4组：对照组（C组），缺硒组（SED组），BPA暴露组(BPA组)和联合暴露组(SeD+BPA组)。该研究检查了焦亡标志物（NLRP3和GSDMD）的表达指标，NF-κB通路相关炎症因子(NF-κB,iNOS,TNF-α,COX-2),焦亡相关因素(ASC，Caspase-1,IL-1β,IL-18),以及样品中的一些热休克蛋白和白细胞介素（HSP60，HSP90，IL-6，IL-17）。结果显示,上述指标的表达在不同治疗组明显上调(P<0.05)。此外,与单独暴露组相比,上述相关指标的表达水平在缺硒和BPA联合暴露组中更显著上调。结论硒缺乏和BPA暴露通过NF-κB/NLRP3/Caspase-1通路诱导鸡气管组织焦亡,BPA暴露会加剧硒缺乏引起的气管焦亡。本研究为与人体微量营养素缺乏和慢性有毒物质共同暴露相关的研究提供了新思路。
