Wang Yong-Sheng, Teng Guo-Qing, Zhou Han
Animal Science and Technology College, Jilin Agricultural Science and Technology University, Jilin, 132101, People's Republic of China.
College of Veterinary Medicine, Northeast Agricultural University, Harbin, 132101, People's Republic of China.
Biol Trace Elem Res. 2021 Apr;199(4):1437-1444. doi: 10.1007/s12011-020-02245-1. Epub 2020 Jun 15.
Selenium (Se) is an essential trace element for both humans and animals. Se deficiency leads to myocardial injury, reproductive disorder, increased exudation, inflammatory injury, and other diseases. The present study analyzed the relationships of Se deficiency, inflammation, and smooth muscle contraction in the small intestine, which is the main tissue that digests and absorbs Se. The model was established by feeding the animals diets with different concentrations of Se. The results showed that the dietary Se content was positively correlated with the blood Se concentration and the intestinal Se concentration. ROS and MPO activity increased with the lack of Se. TNF-α, IL-1β, and IL-6 expression was increased at both the mRNA and protein levels with Se deficiency. The pathways tested showed that the IκBα, NF-κB p65, p38, ERK, and JNK phosphorylation levels were significantly increased with the lack of Se. Moreover, the contractility analysis confirmed that contraction of the intestinal smooth muscle was attenuated by Se deficiency, as shown by the MedLab data acquisition system. These results further illuminated the relationship between inflammation and inhibition of smooth muscle contraction under Se deficiency in the small intestine. The Ca concentration was decreased, and RhoA phosphorylation and ROCK expression were also inhibited by Se deficiency. The results also showed that MLC protein phosphorylation decreased with Se deficiency. In conclusion, the present study indicated that inflammation under Se deficiency leads to the inhibition of smooth muscle contraction in the small intestine.
硒（Se）是人和动物必需的微量元素。缺硒会导致心肌损伤、生殖紊乱、渗出增加、炎症损伤等疾病。本研究分析了缺硒、炎症与小肠平滑肌收缩之间的关系，小肠是消化和吸收硒的主要组织。通过给动物喂食不同硒浓度的日粮来建立模型。结果表明，日粮硒含量与血硒浓度和肠道硒浓度呈正相关。活性氧（ROS）和髓过氧化物酶（MPO）活性随硒缺乏而增加。缺硒时，肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）在mRNA和蛋白水平的表达均增加。所检测的信号通路显示，缺硒时IκBα、核因子-κB p65（NF-κB p65）、p38、细胞外信号调节激酶（ERK）和应激活化蛋白激酶（JNK）的磷酸化水平显著增加。此外，收缩性分析证实，如MedLab数据采集系统所示，缺硒会减弱小肠平滑肌的收缩。这些结果进一步阐明了小肠缺硒时炎症与平滑肌收缩抑制之间的关系。缺硒还会使钙离子浓度降低，抑制RhoA磷酸化和Rho激酶（ROCK）表达。结果还显示，缺硒时肌球蛋白轻链（MLC）蛋白磷酸化减少。总之，本研究表明，缺硒时的炎症会导致小肠平滑肌收缩受到抑制。
