{'fraction_non_alphanumeric': 0.030344202898550724, 'fraction_numerical': 0.014945652173913044, 'mean_word_length': 5.554896142433234, 'pattern_counts': {'":': 0, '<': 3, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
PSVIII-B-14 Peroxisome Proliferator-Activated Receptor Gamma Activation Protects Against Deoxynivalenol-Induced Intestinal Barrier Dysfunction in Jejunal Ipec-J2 Cells


 The role of peroxisome proliferator activated receptor gamma (PPARg) in the regulation of lipid metabolism, adipocyte differentiation and inflammatory response has been well characterized. Besides adipose tissue, PPARg is also highly expressed in the intestine. However, the functional role of PPARg in the regulation of intestinal function still remains poorly understood. In the present study we sought to understand the role of PPARg activation on intestinal barrier function in IPEC-J2 cells exposed (2mM, 24hr) to the mycotoxin, deoxynivalenol (DON). PPARg activation by rosiglitazone and troglitazone dose-dependently increased (P < 0.05) the protein expression of tight junction proteins (TJP), claudin-3 and 4. On the contrary, the protein abundance of claudin-3 and 4 was dose-dependently decreased by PPARg antagonist, T0070907. DON exposure decreased the protein expression of TJP, and also significantly suppressed (P < 0.05) PPARg transcriptional activity. Consistent with the therapeutic benefits of PPARg agonists, pretreatment of cells with PPARg agonists (40 mM) reversed (P < 0.05) the reduction of claudin-3 and 4 induced by DON exposure. Immunofluorescence analysis showed that the decreased membrane presence of claudin-4 and ZO-1 induced by DON was also reversed by troglitazone. Effect of PPARg activation also included partial restoration of transepithelial electrical resistance (TEER) and reduction of FITC-dextran permeability that have been disrupted by DON. However, the protective effects of PPARg agonist against DON exposure was abolished by PPARg antagonist, confirming the importance of PPARg in the observed effects of the agonists. This shows the importance of PPARg activity in the maintenance of intestinal epithelial cells homeostasis and barrier function, especially during periods of metabolic stress induced by the mycotoxin, DON. Therefore, pharmacological and natural bioactive compounds with PPARg agonist activity could be effective in preventing DON-induced gut barrier dysfunction in vivo.