Selenite Stimulates the Proliferation of Intestinal Stem Cells With Elevated Antioxidative Activity.
BACKGROUND
Intestinal stem cells (ISCs) are responsible for the regeneration of intestinal epithelium. In a previous study, we demonstrated that sodium selenite is 1 of the key factors that enhances the growth of ISCs in crypt culture medium. The goal of the present article was to investigate the effect of selenite on the proliferative and antioxidative activities of ISCs.


METHODS
Five-week old BALB/C mice were administered phosphate-buffered saline or sodium selenite (4 mg/kg/d) for 7 days before ISCs were harvested. The proliferative activity of ISC was indexed by the growth of crypt organoids. The messenger RNA expression levels of ISC markers were quantified by using real-time polymerase chain reaction. The activity of antioxidative enzymes was assayed for glutathione peroxidase (GPx), thioredoxin reductase (TrxR), and superoxide dismutase.


RESULTS
Treatment with sodium selenite induced a 1.88-fold increase in the growth number of organoids from ISCs, with elevated expression of leucine-rich repeat-containing G-protein-coupled receptor 5, B lymphoma Moloney murine leukemia virus insertion region homolog-1, and Musashi-1, compared with the ISCs from control samples treated with phosphate-buffered saline. The antioxidative activity of GPx and TrxR was significantly enhanced in the selenite-treated groups (1.55- and 1.23-fold increases, respectively).


CONCLUSIONS
Selenite positively regulated the proliferation of ISCs and activated the expression of ISC markers. The elevated activity of GPx and TrxR induced by selenite should promote the antioxidative ability of ISCs and benefit the growth of organoids.
Department of Surgery, Far Eastern Memorial Hospital, Pan-Chiao, New Taipei, Taiwan, Republic of China; Department of Chemical Engineering and Materials Science, Yuan Ze University, Chung-Li, Taoyuan, Taiwan, Republic of China.
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Chen
Department of Surgery, Far Eastern Memorial Hospital, Pan-Chiao, New Taipei, Taiwan, Republic of China; Department of Chemical Engineering and Materials Science, Yuan Ze University, Chung-Li, Taoyuan, Taiwan, Republic of China. Electronic address: yahuitsi@gmail.com.
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YH
Tsai
Department of Surgery, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, Republic of China. Electronic address: shenghongtseng@gmail.com.
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SH
Tseng
D000818:Animals; D049109:Cell Proliferation / Q000187:drug effects; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D009940:Organoids / Q000187:drug effects*; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D043562:Receptors, G-Protein-Coupled / Q000096:biosynthesis; D020887:Selenious Acid / Q000494:pharmacology*; D013234:Stem Cells / Q000166:cytology / Q000187:drug effects*; D014131:Trace Elements / Q000494:pharmacology*
D012333:RNA, Messenger; D043562:Receptors, G-Protein-Coupled; D014131:Trace Elements; D020887:Selenious Acid