4.6 Article

Selenium deficiency causes apoptosis through endoplasmic reticulum stress in swine small intestine

期刊

BIOFACTORS
卷 47, 期 5, 页码 788-800

出版社

WILEY
DOI: 10.1002/biof.1762

关键词

apoptosis; endoplasmic reticulum stress; IPEC-J2 cells; selenium deficiency; swine small intestine

资金

  1. State key laboratory of animal nutrition [2004DA125184F1725]
  2. earmarked fund for the China Agriculture Research System [CARS35-04]
  3. Key Laboratory of Swine Facilities Engineering of Ministry of Agriculture of China

向作者/读者索取更多资源

This study investigated the mechanism by which selenium deficiency causes intestinal damage in swine, showing that selenium deficiency can induce ER stress, increase apoptosis, and ultimately lead to tissue damage in the small intestine. These results fill the gap in understanding how selenium deficiency induces intestinal injury in swine.
Selenium (Se) plays a crucial role in intestinal health. However, the specific mechanism by which deficiency of Se causes intestinal damage remains unclear. This study was to explore whether Se deficiency can cause ER stress and induce apoptosis in swine small intestine. We established the Se deficiency swine model in vivo and the intestinal epithelial (IPEC-J2) cell Se deficiency model in vitro. The results of morphological observation showed that Se deficiency caused structural damage in intestinal villi and the decrease of goblet cell structure. The apoptotic characteristics such as nucleolar condensation, mitochondrial swelling, and apoptotic bodies were observed in the IPEC-J2 cells. The results of acridine orange/ethidium bromide and mitochondrial membrane potential fluorescence staining in vitro showed that there were more apoptotic cells in the Se-deficiency group than that in the control group. The protein and/or mRNA expression levels of Bax, Bcl-2, caspase 3, caspase 8, caspase 9, cytc, PERK, ATF6, IRE, XBP1, CHOP, GRP78, which are related to ER stress-apoptosis pathway, were significantly increased in the Se-deficient group which compared with the control group in vivo and in vitro were consistent. These results indicated that Se deficiency induced ER stress and increased the apoptosis in swine small intestine and IPEC-J2 cells and then caused the damage in swine small intestinal tissue. Besides, the results of gene expressions in our experiment proved that ER stress induced by Se deficiency promoted apoptosis. These results filled the blank in the mechanism of Se deficiency-induced intestinal injury in swine.

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