Dataset Information

Deoxynivalenol Induces Inflammation in the Small Intestine of Weaned Rabbits by Activating Mitogen-Activated Protein Kinase Signaling.

ABSTRACT: Deoxynivalenol (DON) can activate related signaling pathways and induce gastrointestinal disorders. Based on the results of previous studies, this study tried to explore the relationship between DON-induced intestinal inflammation of weaned rabbits and the ERK-p38 signaling pathway. Forty-five weaned rabbits were divided into three treatments: control, LD and HD group. All rabbits were treated with diet containing a same nutrient content, but animals in the LD and HD groups were additionally administered DON via drinking water at 0.5 and 1.5 mg/kg b.w./d, respectively. The protocol consisted of a total feeding period of 31 days, including a pre-feeding period of 7 days. Western blotting, qRT-PCR, and immunohistochemistry were applied for analysis the expression of protein and mRNA of extracellular signal-regulated kinase (ERK), p38, double-stranded RNA-activated protein kinase (PKR), and hematopoietic cell kinase (Hck) in the duodenum, jejunum, and ileum of rabbits, as well as the distribution of positive reactants. The results proved that DON intake could enhance the levels of inflammatory factors in serum and damage the intestinal structure barrier of rabbits. Meanwhile, DON addition can stimulate the protein and mRNA expression for ERK, p38, PKR, and Hck in the intestine of rabbits, especially in the duodenum, as well as expand the distribution of positive reactants, in a dose-dependent manner.

SUBMITTER: Wang P

PROVIDER: S-EPMC7884333 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature

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Deoxynivalenol Induces Inflammation in the Small Intestine of Weaned Rabbits by Activating Mitogen-Activated Protein Kinase Signaling.

Wang Pengwei P Huang Libo L Yang Wanying W Liu Quancheng Q Li Fuchang F Wang Chunyang C

Frontiers in veterinary science 20210202

Deoxynivalenol (DON) can activate related signaling pathways and induce gastrointestinal disorders. Based on the results of previous studies, this study tried to explore the relationship between DON-induced intestinal inflammation of weaned rabbits and the ERK-p38 signaling pathway. Forty-five weaned rabbits were divided into three treatments: control, LD and HD group. All rabbits were treated with diet containing a same nutrient content, but animals in the LD and HD groups were additionally adm ...[more]

PMID: 33604367

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Project description:Vascular oxidative stress and inflammation play an important role in angiotensin II-induced hypertension, and mitogen-activated protein kinases participate in these processes. We questioned whether mitogen-activated protein kinase-activated protein kinase 2 (MK2), a downstream target of p38 mitogen-activated protein kinase, is involved in angiotensin II-induced vascular responses. In vivo experiments were performed in wild-type and Mk2 knockout mice infused intravenously with angiotensin II. Angiotensin II induced a 30 mm Hg increase in mean blood pressure in wild-type that was delayed in Mk2 knockout mice. Angiotensin II increased superoxide production and vascular cell adhesion molecule-1 in blood vessels of wild-type but not in Mk2 knockout mice. Mk2 knockdown by small interfering RNA in mouse mesenteric vascular smooth muscle cells caused a 42% reduction in MK2 protein and blunted the angiotensin II-induced 40% increase of MK2 expression. Mk2 knockdown blunted angiotensin II-induced doubling of intracellular adhesion molecule-1 expression, 2.4-fold increase of nuclear p65, and 1.4-fold increase in Ets-1. Mk2 knockdown abrogated the angiotensin II-induced 4.7-fold and 1.3-fold increase of monocyte chemoattractant protein-1 mRNA and protein. Angiotensin II enhanced reactive oxygen species levels (by 29%) and nicotinamide adenine dinucleotide phosphate oxidase activity (by 48%), both abolished by Mk2 knockdown. Reduction of MK2 blocked angiotensin II-induced p47phox translocation to the membrane, associated with a 53% enhanced catalase expression. Angiotensin II-induced increase of MK2 was prevented by the nicotinamide adenine dinucleotide phosphate oxidase inhibitor Nox2ds-tat. Mk2 small interfering RNA prevented the angiotensin II-induced 30% increase of proliferation. In conclusion, MK2 plays a critical role in angiotensin II signaling, leading to hypertension, oxidative stress via activation of p47phox and inhibition of antioxidants, and vascular inflammation and proliferation.

Dataset Information

Deoxynivalenol Induces Inflammation in the Small Intestine of Weaned Rabbits by Activating Mitogen-Activated Protein Kinase Signaling.

Publications

Deoxynivalenol Induces Inflammation in the Small Intestine of Weaned Rabbits by Activating Mitogen-Activated Protein Kinase Signaling.

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