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| Effect of β-Caroteneon the Autophagy Mechanism of Intestinal Recess Epithelial Cells IEC-6 Induced by Lipopolysaccharide |
| XU Guang, MA Ti-dong, ZHAO Fan, et al |
| Department of Neonatal Surgery, Hunan Children's Hospital, Changsha Hunan 410007 |
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Abstract 【Objective】To explore the effect of β-Carotene(βC) on the autophagy mechanism of intestinal recess epithelial cells IEC-6induced by lipopolysaccharide.【 Methods 】 The intestinal epithelial cell line IEC-6 was induced by lipopolysaccharide (LPS) to construct the in vitro model of neonatal necrotizing enterocolitis (NEC).The PI3K inhibitor voxtalisib (VOX) was used to analyze the potential mechanism of βC regulating autophagy. IEC-6 cells were divided into control group, LPS group and LPS+βC group and LPS+βC+Vox group after routine culture in vitro. CCC-8 was used to detect cell activity. mRFPGFPLC3 autophagy double labeled adenovirus was transfected to detect intracellular autophagy.The expressions of autophagy related proteins and PI3K/Akt/mTOR signal pathway related proteins were detected by Western blotting.【Rresults】Compared with the control group, the cell activity of LPS group decreased significantly (P<0.05), LC3 Ⅱ/Ⅰ increased significantly (P<0.05), the expression of P62 protein decreased significantly (P<0.05), and the number of autophagy spots increased significantly (P<0.05). Compared with the control group, the cell activity in the LPS+βC group increased significantly (P<0.05), LC3 Ⅱ/Ⅰ decreased significantly (P<0.05), the protein expression of P62 increased significantly (P<0.05), and the number of autophagy spots decreased significantly (P<0.05). Compared with the LPS group, the cell activity in the LPS+βC group increased significantly (P<0.05), LC3 Ⅱ/Ⅰ decreased significantly (P<0.05). The protein expression of P62, p-PI3K, p-AKT and p-mTOR increased significantly (P<0.05), and the number of autophagy spots decreased significantly (P<0.05). 【Conclusion】 βC can reduce the autophagy of IEC-6 cells induced by LPS, and its mechanism is related to the activation of PI3K/AKT/mTOR signaling pathway.
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Received: 17 January 2022
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2022, Vol. 39 
