Se Deficiency Induced Inflammation Resulting to a Diminished Contraction of the Small Intestinal Smooth Muscle in Mice.

Abstract

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 Ca2+ 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.