Global Health Institute, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, 712000, China; Department of Occupational and Environmental Health, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China; Key Laboratory of Environment and Genes Related to Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.
Global Health Institute, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, 712000, China; Department of Occupational and Environmental Health, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China; Key Laboratory of Environment and Genes Related to Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China; Xi'an Gem Flower Chang Qing Hospital, Xi'an 710200, China.
Int Immunopharmacol. 2024 Mar 30;130:111574. doi: 10.1016/j.intimp.2024.111574. Epub 2024 Feb 16.
Selenium (Se) is a trace element necessary for humans to maintain normal physiological activities, and Se deficiency may lead to splenic injury, while Se supplementation can alleviate splenic injury. However, the mechanism is unclear. In this study, we constructed a Se deficiency animal model by feeding Sprague-Dawley (SD) rats with low Se feed. Meanwhile, we observed the repairing effect of Se supplementation on splenic injury with two doses of novel nano-selenium (Nano-Se) supplement by gavage. We measured the Se content in the spleens of the rats by atomic fluorescence spectroscopy (AFS) method and combined the results of hematoxylin-eosin (HE) and Masson staining to observe the splenic injury, comprehensively evaluating the construction of the animal model of low selenium-induced splenic injury. We measured the mRNA and protein expression levels of p38 mitogen-activated protein kinase (p38 MAPK), nuclear factor kappa-B (NF-κB), and interleukin-6 (IL-6) in the spleen by Real-time quantitative polymerase chain reaction (qPCR), western blot (WB), and immunohistochemistry (IHC). We found that the Se deficiency group exhibited lower Se content, splenic fibrosis, and high expression of p38 MAPK, NF-κB, and IL-6 compared to the normal group. The Se supplement groups exhibited higher Se content, attenuated splenic injury, and down-regulated expression of p38 MAPK, NF-κB, and IL-6 relative to the Se deficiency group. This study suggests that Se deficiency leads to splenic injury in rats, and Se supplementation may attenuate splenic injury by inhibiting the expression of p38 MAPK, NF-κB and IL-6.
硒（Se）是人体维持正常生理活动所必需的微量元素，硒缺乏可能导致脾脏损伤，而补硒可以减轻脾脏损伤。然而，其机制尚不清楚。在本研究中，我们通过用低硒饲料喂养 Sprague-Dawley（SD）大鼠构建了硒缺乏动物模型。同时，我们通过灌胃两种剂量的新型纳米硒（Nano-Se）补充剂来观察硒补充对脾脏损伤的修复作用。我们通过原子荧光光谱法（AFS）测量大鼠脾脏中的硒含量，并结合苏木精-伊红（HE）和 Masson 染色的结果观察脾脏损伤，综合评价低硒诱导的脾脏损伤动物模型的构建。我们通过实时定量聚合酶链反应（qPCR）、western blot（WB）和免疫组织化学（IHC）测量脾脏中 p38 丝裂原活化蛋白激酶（p38 MAPK）、核因子 kappa-B（NF-κB）和白细胞介素-6（IL-6）的 mRNA 和蛋白表达水平。我们发现，与正常组相比，硒缺乏组的 Se 含量较低，脾脏纤维化程度较高，p38 MAPK、NF-κB 和 IL-6 的表达水平较高。与硒缺乏组相比，硒补充组的 Se 含量较高，脾脏损伤程度减轻，p38 MAPK、NF-κB 和 IL-6 的表达水平下调。本研究表明，硒缺乏可导致大鼠脾脏损伤，而硒补充可能通过抑制 p38 MAPK、NF-κB 和 IL-6 的表达来减轻脾脏损伤。
