ArticleBMC gastroenterology2026
ITPR1 mediates the PI3K/AKT/mTOR pathway to regulate cellular autophagy, affecting lipopolysaccharide-induced pediatric inflammatory bowel disease.
Article in BMC gastroenterology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPediatric inflammatory bowel disease (PIBD) is a complex and far-reaching chronic intestinal disorder that poses major challenges to the growth, development, and quality of life of children. Inositol 1,4,5-trisphosphate receptor type 1 (ITPR1) is a key intracellular calcium channel protein that plays important roles in a wide range of biological processes. However, the role and potential mechanism of action of ITPR1 in PIBD remain unclear. This study aimed to reveal the effects and potential mechanisms of ITPR1 expression in a cell model of PIBD.
methodsNCM460 cells were treated with lipopolysaccharide (LPS) to construct the cell model, and the cells were transfected with a small interfering RNA targeting ITPR1. The effects of LPS and ITPR1 on the viability and inflammatory response of NCM460 cells were analyzed by observing the proliferative viability of NCM460 cells and the secretion of inflammatory factors. The expression levels of autophagy-related proteins were analyzed using LC3 fluorescent labeling and western blotting (WB) experiments to reveal the effects of ITPR1 on LPS-induced autophagy in NCM460 cells. Finally, PI3K/AKT/mTOR phosphorylation levels were detected using WB, and the effects of the PI3K pathway on LPS-induced autophagy and inflammatory responses in NCM460 cells were analyzed in combination with the PI3K pathway inhibitor, LY294002.
resultsLPS significantly increased the mRNA (P < 0.0001) and protein (P < 0.01) expression level of ITPR1 in NCM460 cells. LPS significantly inhibited the proliferative activity of NCM460 cells and promoted the secretion of inflammatory factors (all P < 0.001). In addition, the level of autophagy in NCM460 cells was remarkably increased (P < 0.001) and the phosphorylation levels of PI3K, AKT and mTOR (all P < 0.001) were markedly inhibited after LPS induction. Interference with ITPR1 expression in the cells reversed these results, but this reversal was, in turn, noticeably reversed by LY294002.
conclusionsOur results confirmed that ITPR1 silencing inhibited the LPS-induced reduction in cell viability, inflammation, and autophagy through the reactivation of the PI3K/AKT/mTOR pathway, suggesting a potential candidate target for the treatment of PIBD.
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