Protective Effect of Ganoderma atrum Polysaccharide on Lipopolysaccharide-induced Damage in Intestinal Epithelial Cell IEC-6

被引:0
作者
Zheng B. [1 ]
Hu X. [1 ]
Chen Y. [1 ]
Xie J. [1 ]
Yu Q. [1 ]
机构
[1] State Key Laboratory of Food Science and Resources, Nanchang University, China-Canada Joint Lab of Food Science and Technology (Nanchang), Nanchang
关键词
apoptosis; cell migration; Ganoderma atrum polysaccharide; intestinal epithelial cells (IEC-6); lipopolysaccharide;
D O I
10.16429/j.1009-7848.2024.04.005
中图分类号
学科分类号
摘要
Objective: To investigate the protective effect of Ganoderma atrum polysaccharide (PSG -1) against lipopolysaccharide (LPS)-induced damage in intestinal epithelial cell (IEC-6) and its underlying mechanisms. Methods: The intervention effects of PSG-1 on IEC-6 cells were investigated using a LPS-induced intestinal epithelial cell IEC-6 injury model, and the effect of PSG-1 intervention on cell viability was assessed using the cell counting kit-8 (CCK-8) assay. Western blot technology was employed to investigate the alterations in the expression of intestinal tight junction proteins and cyclooxygenase-2 (cox-2) in the cells. Transcriptome sequencing analysis was conducted to explore the potential protective mechanisms of PSG-1, followed by experimental validation. Results: Intervention with PSG-1 significantly enhanced cell viability and the expression of intestinal barrier proteins, including ZO-1, Claudin-1, and Occludin. Moreover, PSG-1 exhibited an inhibitory effect on the abnormal upregulation ofcox-2 induced by LPS. Transcriptome sequencing analysis, scratch assay, and western blot experiments validation demonstrated that PSG-1 significantly enhanced cell migration ability while suppressing the expression of pro-apoptotic proteins, including Bax, Caspase-3, and Caspase-9. Conclusion; PSG-1 exhibited significant improvement in LPS-induced damage in IEC-6 cell. Cell migration and apop-tosis might be key mechanisms through which PSG-1 exerted its protective effects. © 2024 Chinese Institute of Food Science and Technology. All rights reserved.
引用
收藏
页码:43 / 53
页数:10
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