Selenium deficiency induced apoptosis via mitochondrial pathway caused by Oxidative Stress in porcine gastric tissues

Abstract

Selenium (Se) is an essential nutrient for the body, which can ensure GSH-Px activity and has antioxidant effect. Se deficiency may lead to apoptosis in various tissues and organs in animals. Pigs as major livestock in the farming industry, Se deficiency can cause various types of diseases such as white muscle disease, and mulberry heart disease.The aim of this experiment was to investigate the effect and mechanism of Se deficiency on apoptosis in porcine gastric tissue. Forty weaned piglets were randomly divided into Se deficiency group and control group, and fed with low Se diet and normal diet for six weeks respectively. The histochemical characteristics, antioxidant indexes, apoptotic genes and apoptotic protein expression of gastric cells in Se-deficient piglets were detected. The results of antioxidant index, TUNEL, RT-PCR and Western blot showed that Se deficiency decreased the activities of CAT, SOD and GSH-Px, increased the apoptotic rate of porcine gastric tissue, increased the expression of Bax and Caspase-3, and decreased the expression of Bcl-2. The results demonstrated that Se deficiency could induce apoptosis in porcine gastric tissue cells through oxidative stress-induced mitochondrial pathway. The stomach was a key target of Se deficiency and may play a key role in the response to Se deficiency. Our study may provide new ideas for the prevention and treatment of swine gastric diseases caused by Se deficiency and is beneficial to the development of pig farming industry