Environmental Health and Disease Laboratory, Department of Environmental Health Sciences, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA; Department of Family and Community Medicine, College of Medicine, Taibah University, Madinah, Saudi Arabia.
Environmental Health and Disease Laboratory, Department of Environmental Health Sciences, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA.
Environ Toxicol Pharmacol. 2020 Nov;80:103457. doi: 10.1016/j.etap.2020.103457. Epub 2020 Jul 17.
Evidence from pediatric studies show that infants and children are at risk for early exposure to microcystin. The present report tests the hypothesis that early life exposure to microcystin (MC), a principal component of harmful algal blooms followed by a juvenile exposure to high-fat diet feeding potentiate the development of nonalcoholic fatty liver disease phenotype in adulthood. Results showed classical symptoms of early NAFLD linked inflammation. Cytokines and chemokines such as CD68, IL-1β, MCP-1, and TNF-α, as well as α-SMA were increased in the groups that were exposed to MC-LR with the high-fat diet compared to the vehicle group. Also, mechanistically, NLRP3 KO mice showed a significant decrease in the inflammation and NAFLD phenotype and resisted the metabolic changes such as insulin resistance and glucose metabolism in the liver. The data suggested that MC-LR exposure and subsequent NLRP3 inflammasome activation in childhood could impact liver health in juveniles.
儿科研究证据表明，婴儿和儿童面临早期接触微囊藻毒素的风险。本报告检验了以下假设：即生命早期接触微囊藻毒素（MC）——有害藻类大量繁殖的主要成分，随后在青少年时期接触高脂肪饮食，会促进成年后非酒精性脂肪性肝病表型的发展。结果显示出与早期非酒精性脂肪性肝病相关的炎症的典型症状。与载体组相比，暴露于 MC-LR 加高脂肪饮食的组中，细胞因子和趋化因子（如 CD68、IL-1β、MCP-1 和 TNF-α）以及α-SMA 增加。此外，从机制上讲，NLRP3 KO 小鼠的炎症和非酒精性脂肪性肝病表型显著减少，并抵抗了肝脏中的胰岛素抵抗和葡萄糖代谢等代谢变化。数据表明，MC-LR 暴露和随后 NLRP3 炎性体激活在儿童时期可能会影响青少年的肝脏健康。
