Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 41, Issue 2, Pages 623-634Publisher
KARGER
DOI: 10.1159/000457933
Keywords
P38 MAPK; SB203580; Total parenteral nutrition; Intestinal barrier; Lipoapoptosis
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Funding
- Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition [14DZ2272400]
- Shanghai Municipal Commission of Health and Family Planning [201640264]
- National Natural Science Foundation of China [81400861, 81630039]
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Background & Aims: Our previous studies have provided evidence that p38 mitogenactivated protein kinase (MAPK) is involved in total parenteral nutrition (TPN)-associated complications, but its exact effects and mechanisms have not been fully understood. This study aimed to evaluate the roles of p38 MAPK inhibitor SB203580 in the TPN-induced loss of intestinal barrier function and liver disease. Methods: A rodent model of TPN was used to analyze the roles of SB203580 in TPN-associated complications. Intestinal barrier function was evaluated by transepithelial electrical resistance (TER) and paracellular permeability in Caco-2 cells. The palmitic acid (PA) was used to induce hepatic lipoapoptosis in vitro. The lipoapoptosis was detected using Caspase-3/7 and lipid staining. Results: In the present study, we showed that SB203580 treatment significantly suppressed TPN-mediated intestinal permeability in rats. SB203580 treatment significantly inhibited IL-1 beta-induced an increase in tight junction permeability of Caco-2 cells via repressing the p38/ATF-2 signaling. Unexpectedly, SB203580 treatment enhanced hepatic lipoapoptosis in the model of TPN. Palmitic acid (PA)-induced hepatic lipoapoptosis in human liver cells was significantly augmented by the SB203580 treatment. Conclusions: We demonstrate that the p38 MAPK inhibitor SB203508 ameliorates intestinal barrier function but promotes hepatic lipoapoptosis in model of TPN. (C) 2017 The Author(s) Published by S. Karger AG, Basel
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