College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China.
College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China.
Comp Biochem Physiol C Toxicol Pharmacol. 2023 Jan;263:109488. doi: 10.1016/j.cbpc.2022.109488. Epub 2022 Oct 17.
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.
硒缺乏可导致体内多组织器官损伤，且可能与慢性毒性暴露共存。双酚 A（BPA）暴露污染可诱导多种损伤的发生，包括细胞焦亡。然而，目前尚不清楚硒缺乏和 BPA 暴露是否会影响鸡的气管组织细胞焦亡。为了研究硒缺乏和 BPA 暴露是否通过 NF-κB/NLRP3/Caspase-1 途径诱导鸡气管组织细胞焦亡，以及它们联合暴露对组织损伤的影响，我们建立了相关鸡气管损伤模型。将 60 只肉鸡分为 4 组：对照组（C 组）、硒缺乏组（SeD 组）、BPA 暴露组（BPA 组）和联合暴露组（SeD+BPA 组）。研究检测了细胞焦亡标志物（NLRP3&GSDMD）、NF-κB 通路相关炎症因子（NF-κB、iNOS、TNF-α、COX-2）、细胞焦亡相关因子（ASC、Caspase-1、IL-1β、IL-18）以及一些热休克蛋白和白细胞介素（HSP60、HSP90、IL-6、IL-17）在样本中的表达指标。结果表明，不同处理组上述指标表达均显著上调（P<0.05）。此外，联合硒缺乏和 BPA 暴露组上述相关指标的表达水平较单独暴露组显著上调。结论：硒缺乏和 BPA 暴露通过 NF-κB/NLRP3/Caspase-1 途径诱导鸡气管组织细胞焦亡，BPA 暴露加剧了硒缺乏诱导的气管细胞焦亡。本研究为研究机体微量营养素缺乏与慢性毒物的共同暴露提供了新的思路。
