Abstract
Deoxynivalenol (DON) is the most common mycotoxin that frequently contaminates human food and animal feed, resulting in intestinal diseases and systemic immunosuppression. Glycyrrhinic acid (GA) exhibits various pharmacological activities. To investigate the protective mechanism of GA for DON-induced inflammation and apoptosis in IPEC-J2 cells, RNA-seq analysis was used in the current study. The IPEC-J2 cells were treated with the control group (CON), 0.5 μg/mL DON, 400 μg/mL GA, and 400 μg/mL GA+0.5 μg/mL DON (GAD) for 6 h. Results showed that 0.5 μg/mL DON exposure for 6 h could induce oxidative stress, inflammation, and apoptosis in IPEC-J2 cells. GA addition could specifically promote the proliferation of DON-induced IPEC-J2 cells in a dose- and time-dependent manner. In addition, GA addition significantly increased Bcl-2 gene expression (P < 0.05) and superoxide dismutase and catalase activities (P < 0.01) and decreased lactate dehydrogenase release, the contents of malonaldehyde, IL-8, and NF-κB (P < 0.05), the relative mRNA abundances of IL-6, IL-8, TNF-α, COX-2, NF-κB, Bax, and caspase 3 (P < 0.01), and the protein expressions of Bax and TNF-α. Moreover, a total of 1576, 289, 1398, and 154 differentially expressed genes were identified in CON vs. DON, CON vs. GA, CON vs. GAD, and DON vs. GAD, respectively. Transcriptome analysis revealed that MAPK, TNF, and NF-κB signaling pathways and some chemokines played significant roles in the regulation of inflammation and apoptosis induced by DON. GA may alleviate DON cytotoxicity via the TNF signaling pathway by downregulating IL-15, CCL5, and other gene expressions. These results indicated that GA could alleviate DON-induced oxidative stress, inflammation, and apoptosis via the TNF signaling pathway in IPEC-J2 cells.
Highlights
The gastrointestinal tract of animals plays an important role in the digestion and absorption of various nutrients and provides a pivotal barrier against food contaminants and other harmful irritants such as toxins, stress, and pathogens [1, 2]
Consumption of DONcontaminated food or feed brings about the compromised intestinal epithelial barrier function [6], the augment of Oxidative Medicine and Cellular Longevity intestinal permeability [7], disordered intestinal structure [8], and lower nutrient absorption [9], which leads to intestinal diseases and systemic immunosuppression
Annexin V-FITC/PI staining further confirmed that Glycyrrhinic acid (GA) significantly decreased cell apoptosis induced by DON
Summary
The gastrointestinal tract of animals plays an important role in the digestion and absorption of various nutrients and provides a pivotal barrier against food contaminants and other harmful irritants such as toxins, stress, and pathogens [1, 2]. The injury gastrointestinal tract will cause barrier dysfunction, leading to inflammatory bowel diseases, necrotizing enterocolitis, and other intestinal diseases [3]. Consumption of DONcontaminated food or feed brings about the compromised intestinal epithelial barrier function [6], the augment of Oxidative Medicine and Cellular Longevity intestinal permeability [7], disordered intestinal structure [8], and lower nutrient absorption [9], which leads to intestinal diseases and systemic immunosuppression. The IPEC-J2 cell line, isolated from the jejunal epithelium of the neonatal piglet, was widely used as an in vitro model for studying intestinal functions [10]
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