由于其潜在的不良健康影响,暴露于丙烯酸酰胺(AD)引起了全世界的关注,促使世界卫生组织呼吁加强对相关风险的研究。尽管如此,口服丙烯酸酰胺(丙烯酰胺)(AD)暴露与肺功能障碍之间的关系仍然知之甚少。我们的研究旨在探讨口腔内暴露于AD与肺功能下降之间的相关性。在探索组织炎症等潜在介导因素的同时,氧化应激,焦亡,和凋亡。此外,我们旨在评估氧化锌纳米颗粒绿色合成辣木提取物(ZNO-MONP)(10mg/kgb.wt)对ACR毒性的潜在保护作用,并进行了全面的miRNA表达谱分析,以揭示AD毒性的新靶标和机制(miRNA223-3P和miRNA325-3P)。此外,我们使用计算技术来预测丙烯酸酰胺和/或MO提取物成分与组织蛋白之间的相互作用。使用大鼠模型,我们将动物暴露于口服丙烯酰胺(20mg/kgb.wt,持续2个月)。我们的发现表明AD显著下调miRNA223-3P和miRNA325-3P的表达,针对NLRP-3和GSDMD,分别,表明通过炎症小体激活途径诱导肺组织中的焦亡。此外,AD暴露导致脂质过氧化损伤和GPX水平降低,CAT,GSH,和GSSG。值得注意的是,AD暴露上调凋亡,热解,和炎症基因,伴有肺组织病理损伤。免疫组织化学和免疫荧光技术检测到包括波形蛋白和4HNE在内的指示性有害蛋白水平升高。相反,ZNO-MONP与AD的同时给药显著升高miRNA223-3P和miRNA325-3P的表达,保护免受氧化应激,凋亡,焦亡,炎症,和大鼠肺纤维化。总之,我们的研究强调了ZNO-MONPs在保护肺组织免受食源性毒素AD有害影响方面的功效.
Exposure to acrylic amide (AD) has garnered worldwide attention due to its potential adverse health effects, prompting calls from the World Health Organization for intensified research into associated risks. Despite this, the relationship between oral acrylic amide (acrylamide) (AD) exposure and pulmonary dysfunction remains poorly understood. Our study aimed to investigate the correlation between internal oral exposure to AD and the decline in lung function, while exploring potential mediating factors such as tissue inflammation, oxidative stress, pyroptosis, and apoptosis. Additionally, we aimed to evaluate the potential protective effect of zinc oxide nanoparticles green-synthesized moringa extract (ZNO-MONPs) (10 mg/kg b.wt) against ACR toxicity and conducted comprehensive miRNA expression profiling to uncover novel targets and mechanisms of AD toxicity (miRNA 223-3 P and miRNA 325-3 P). Furthermore, we employed computational techniques to predict the interactions between acrylic amide and/or MO-extract components and tissue proteins. Using a rat model, we exposed animals to oral acrylamide (20 mg/kg b.wt for 2 months). Our findings revealed that AD significantly downregulated the expression of miRNA 223-3 P and miRNA 325-3 P, targeting NLRP-3 & GSDMD, respectively, indicating the induction of pyroptosis in pulmonary tissue via an inflammasome activating pathway. Moreover, AD exposure resulted in lipid peroxidative damage and reduced levels of GPX, CAT, GSH, and GSSG. Notably, AD exposure upregulated apoptotic, pyroptotic, and inflammatory genes, accompanied by histopathological damage in lung tissue. Immunohistochemical and immunofluorescence techniques detected elevated levels of indicative harmful proteins including vimentin and 4HNE. Conversely, concurrent administration of ZNO-MONPs with AD significantly elevated the expression of miRNA 223-3 P and miRNA 325-3 P, protecting against oxidative stress, apoptosis, pyroptosis, inflammation, and fibrosis in rat lungs. In conclusion, our study highlights the efficacy of ZNO-MONPs NPs in protecting pulmonary tissue against the detrimental impacts of foodborne toxin AD.