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Article: Autophagy in intestinal fibrosis: relevance in inflammatory bowel disease.

Macias-Ceja, Dulce C / Barrachina, María D / Ortiz-Masià, Dolores

2023 Volume 14, Page(s) 1170436

Abstract: Chronic inflammation is often associated with fibrotic disorders in which an excessive deposition of extracellular matrix is a hallmark. Long-term fibrosis starts with tissue hypofunction and finally ends in organ failure. Intestinal fibrosis is not an ... ...

Abstract	Chronic inflammation is often associated with fibrotic disorders in which an excessive deposition of extracellular matrix is a hallmark. Long-term fibrosis starts with tissue hypofunction and finally ends in organ failure. Intestinal fibrosis is not an exception, and it is a frequent complication of inflammatory bowel disease (IBD). Several studies have confirmed the link between deregulated autophagy and fibrosis and the presence of common prognostic markers; indeed, both up- and downregulation of autophagy are presumed to be implicated in the progression of fibrosis. A better knowledge of the role of autophagy in fibrosis may lead to it becoming a potential target of antifibrotic therapy. In this review we explore novel advances in the field that highlight the relevance of autophagy in fibrosis, and give special focus to fibrosis in IBD patients.
Language	English
Publishing date	2023-06-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2023.1170436
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Article: SUCNR1 Mediates the Priming Step of the Inflammasome in Intestinal Epithelial Cells: Relevance in Ulcerative Colitis.

Bauset, Cristina / Lis-Lopez, Lluis / Coll, Sandra / Gisbert-Ferrándiz, Laura / Macias-Ceja, Dulce C / Seco-Cervera, Marta / Navarro, Francisco / Esplugues, Juan V / Calatayud, Sara / Ortiz-Masia, Dolores / Barrachina, Maria D / Cosín-Roger, Jesús

Biomedicines

2022 Volume 10, Issue 3

Abstract: Intestinal epithelial cells (IECs) constitute a defensive physical barrier in mucosal tissues and their disruption is involved in the etiopathogenesis of several inflammatory pathologies, such as Ulcerative Colitis (UC). Recently, the succinate receptor ... ...

Abstract	Intestinal epithelial cells (IECs) constitute a defensive physical barrier in mucosal tissues and their disruption is involved in the etiopathogenesis of several inflammatory pathologies, such as Ulcerative Colitis (UC). Recently, the succinate receptor SUCNR1 was associated with the activation of inflammatory pathways in several cell types, but little is known about its role in IECs. We aimed to analyze the role of SUCNR1 in the inflammasome priming and its relevance in UC. Inflammatory and inflammasome markers and SUCNR1 were analyzed in HT29 cells treated with succinate and/or an inflammatory cocktail and transfected with SUCNR1 siRNA in a murine DSS model, and in intestinal resections from 15 UC and non-IBD patients. Results showed that this receptor mediated the inflammasome, priming both in vitro in HT29 cells and in vivo in a murine chronic DSS-colitis model. Moreover, SUNCR1 was also found to be involved in the activation of the inflammatory pathways NFкB and ERK pathways, even in basal conditions, since the transient knock-down of this receptor significantly reduced the constitutive levels of pERK-1/2 and pNFкB and impaired LPS-induced inflammation. Finally, UC patients showed a significant increase in the expression of SUCNR1 and several inflammasome components which correlated positively and significantly. Therefore, our results demonstrated a role for SUCNR1 in basal and stimulated inflammatory pathways in intestinal epithelial cells and suggested a pivotal role for this receptor in inflammasome activation in UC.
Language	English
Publishing date	2022-02-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10030532
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Article: IFNγ-Treated Macrophages Induce EMT through the WNT Pathway: Relevance in Crohn's Disease.

Macias-Ceja, Dulce C / Coll, Sandra / Bauset, Cristina / Seco-Cervera, Marta / Gisbert-Ferrándiz, Laura / Navarro, Francisco / Cosin-Roger, Jesus / Calatayud, Sara / Barrachina, María D / Ortiz-Masia, Dolores

Biomedicines

2022 Volume 10, Issue 5

Abstract: Background: Fibrosis is a common complication of Crohn's disease (CD) in which macrophages play a central role. Epithelial-mesenchymal transition (EMT) and the WNT pathway have been associated with fibrosis. We aim to analyse the relevance of the tissue ...

Abstract	Background: Fibrosis is a common complication of Crohn's disease (CD) in which macrophages play a central role. Epithelial-mesenchymal transition (EMT) and the WNT pathway have been associated with fibrosis. We aim to analyse the relevance of the tissue microenvironment in macrophage phenotype and the EMT process. Methods: Intestinal surgical resections are obtained from control and CD patients with stenotic or penetrating behaviour. Cytokine's expression, macrophage phenotype, EMT markers and WNT signalling pathway are determined by WB, RT-PCR, ELISA or Cytometry. U937 cells are treated with IFNγ, TNFα, IL1β, IL4 or IL10 and co-cultured with HT29 cells and, in some cases, are treated with XAV939 or Results: IFNγ, WNT6, CD16 and CD86 are increased in the intestinal tissue of CD patients. IFNγ-treated U937 activated the EMT process and WNT pathway in HT29 cells, and the EMT process is mediated by FZD4. Conclusions: An IFNγ-rich microenvironment polarises macrophages, which induces EMT through the WNT pathway.
Language	English
Publishing date	2022-05-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10051093
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Article ; Online: Diminished Vitamin D Receptor Protein Levels in Crohn's Disease Fibroblasts: Effects of Vitamin D.

Gisbert-Ferrándiz, Laura / Cosín-Roger, Jesús / Hernández, Carlos / Macias-Ceja, Dulce C / Ortiz-Masiá, Dolores / Salvador, Pedro / Esplugues, Juan V / Hinojosa, Joaquín / Navarro, Francisco / Calatayud, Sara / Barrachina, María D

Nutrients

2020 Volume 12, Issue 4

Abstract: Vitamin D (VD) deficiency has been associated to Crohn's disease (CD) pathogenesis, and the exogenous administration of VD improves the course of the disease, but the mechanistic basis of these observations remains unknown. Vitamin D receptor (VDR) ... ...

Abstract	Vitamin D (VD) deficiency has been associated to Crohn's disease (CD) pathogenesis, and the exogenous administration of VD improves the course of the disease, but the mechanistic basis of these observations remains unknown. Vitamin D receptor (VDR) mediates most of the biological functions of this hormone, and we aim to analyze here the expression of VDR in intestinal tissue, epithelial cells, and fibroblasts from CD patients. The effects of VD on a fibroblast wound healing assay and murine intestinal fibrosis are also analyzed. Our data show diminished VDR protein levels in surgical resections and epithelial cells from CD patients. In intestinal fibroblasts isolated from damaged tissue of CD patients, we detected enhanced migration and decreased VDR expression compared with both fibroblasts from non-damaged tissue of the same CD patient or control fibroblasts. Treatment with VD increased VDR protein levels, avoided the accelerated migration in CD fibroblasts, and prevented murine intestinal fibrosis induced by the heterotopic transplant model. In conclusion, our study demonstrates diminished VDR protein levels associated with enhanced migration in intestinal fibroblasts from damaged tissue of CD patients. In these cells, VD accumulates VDR and normalizes migration, which supports that CD patients would benefit from the VD anti-fibrotic therapeutic value that we demonstrate in a murine experimental model.
MeSH term(s)	Animals ; Cell Movement/drug effects ; Crohn Disease/drug therapy ; Crohn Disease/etiology ; Crohn Disease/metabolism ; Crohn Disease/pathology ; Disease Models, Animal ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Female ; Fibroblasts/metabolism ; Fibroblasts/physiology ; Fibrosis ; Gene Expression Regulation/drug effects ; Humans ; Intestines/cytology ; Intestines/pathology ; Male ; Mice, Inbred C57BL ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/metabolism ; Vitamin D/pharmacology ; Vitamin D/therapeutic use ; Vitamin D Deficiency/complications ; Wound Healing/drug effects
Chemical Substances	Receptors, Calcitriol ; Vitamin D (1406-16-2)
Language	English
Publishing date	2020-04-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu12040973
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Article ; Online: Succinate Activates EMT in Intestinal Epithelial Cells through SUCNR1: A Novel Protagonist in Fistula Development.

Ortiz-Masiá, Dolores / Gisbert-Ferrándiz, Laura / Bauset, Cristina / Coll, Sandra / Mamie, Céline / Scharl, Michael / Esplugues, Juan V / Alós, Rafael / Navarro, Francisco / Cosín-Roger, Jesús / Barrachina, María D / Calatayud, Sara

Cells

2020 Volume 9, Issue 5

Abstract: The pathogenesis of Crohn's disease-associated fibrostenosis and fistulas imply the epithelial-to-mesenchymal transition (EMT) process. As succinate and its receptor (SUCNR1) are involved in intestinal inflammation and fibrosis, we investigated their ... ...

Abstract	The pathogenesis of Crohn's disease-associated fibrostenosis and fistulas imply the epithelial-to-mesenchymal transition (EMT) process. As succinate and its receptor (SUCNR1) are involved in intestinal inflammation and fibrosis, we investigated their relevance in EMT and Crohn's disease (CD) fistulas. Succinate levels and SUCNR1-expression were analyzed in intestinal resections from non-Inflammatory Bowel Disease (non-IBD) subjects and CD patients with stenosing-B2 or penetrating-B3 complications and in a murine heterotopic-transplant model of intestinal fibrosis. EMT, as increased expression of Snail1, Snail2 and vimentin and reduction in E-cadherin, was analyzed in tissues and succinate-treated HT29 cells. The role played by SUCNR1 was studied by silencing its gene. Succinate levels and SUCNR1 expression are increased in B3-CD patients and correlate with EMT markers. SUCNR1 is detected in transitional cells lining the fistula tract and in surrounding mesenchymal cells. Grafts from wild type (WT) mice present increased succinate levels, SUCNR1 up-regulation and EMT activation, effects not observed in SUCNR1
MeSH term(s)	Animals ; Cadherins/metabolism ; Crohn Disease/drug therapy ; Crohn Disease/genetics ; Crohn Disease/metabolism ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Fibrosis/drug therapy ; Fibrosis/metabolism ; Fistula/drug therapy ; Fistula/pathology ; Humans ; Inflammation/drug therapy ; Inflammation/pathology ; Intestines/drug effects ; Intestines/pathology ; Receptors, G-Protein-Coupled/drug effects ; Succinic Acid/metabolism ; Succinic Acid/pharmacology
Chemical Substances	Cadherins ; Receptors, G-Protein-Coupled ; SUCNR1 protein, human ; Succinic Acid (AB6MNQ6J6L)
Language	English
Publishing date	2020-04-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9051104
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Article ; Online: The vitamin D receptor Taq I polymorphism is associated with reduced VDR and increased PDIA3 protein levels in human intestinal fibroblasts.

Gisbert-Ferrándiz, Laura / Cosin-Roger, Jesus / Hernández, Carlos / Macias-Ceja, Dulce C / Ortiz-Masiá, Dolores / Salvador, Pedro / Wildenberg, M E / Esplugues, Juan V / Alós, Rafael / Navarro, Francisco / Calatayud, Sara / Barrachina, María D

The Journal of steroid biochemistry and molecular biology

2020 Volume 202, Page(s) 105720

Abstract: The synonymous single nucleotide polymorphism (SNP) rs731236, located in the vitamin D receptor (VDR) gene (Taq I) has been associated with both decreased levels of the protein in peripheral blood mononuclear cells and a fibrosis-related complication in ... ...

Abstract	The synonymous single nucleotide polymorphism (SNP) rs731236, located in the vitamin D receptor (VDR) gene (Taq I) has been associated with both decreased levels of the protein in peripheral blood mononuclear cells and a fibrosis-related complication in Crohn´s disease (CD). Interactions between VDR and a protein-disulfide isomerase-associated 3 (PDIA3) in the regulation of extracellular matrix have been reported and we aim to analyze the relevance of the VDR genotypes and the effects of Vitamin D (VD) in the expression of VDR, PDIA3 and proliferation of intestinal fibroblasts. Human intestinal fibroblasts were isolated from the non-affected surgical resections of colorectal patients and classified according to the VDR genotype. In some cases, cells were transfected with specific PDIA3 siRNA. Basal and VD-stimulated expression of VDR, PDIA3 and Collagen 1A1 (COL1A1) as well as fibroblast migration/proliferation were analyzed. Our data show that intestinal fibroblasts homozygous for the C allele in the VDR gene exhibited lower VDR protein levels and higher proliferation than cells homozygous for the T allele. VD increased VDR and attenuated the accelerated proliferation of CC fibroblasts. The diminished VDR level detected in CC cells was associated with increased levels of both PDIA3 and COL1A1 expression and the transient silencing of PDIA3 significantly reduced COL1A1 expression. We conclude that intestinal fibroblasts homozygous for the C allele in the VDR gene exhibited: reduced VDR protein levels, increased proliferation and increased PDIA3/COL1A1 expression. Treatment with VD increased VDR and attenuated proliferation of these cells.
MeSH term(s)	Adolescent ; Adult ; Alleles ; Cell Proliferation ; Cells, Cultured ; Female ; Fibroblasts/metabolism ; Genotype ; Humans ; Intestines/cytology ; Male ; Polymorphism, Single Nucleotide ; Protein Disulfide-Isomerases/metabolism ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/metabolism ; Young Adult
Chemical Substances	Receptors, Calcitriol ; VDR protein, human ; Protein Disulfide-Isomerases (EC 5.3.4.1) ; PDIA3 protein, human (EC 5.3.4.1.)
Language	English
Publishing date	2020-06-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1049188-0
ISSN	1879-1220 ; 0960-0760
ISSN (online)	1879-1220
ISSN	0960-0760
DOI	10.1016/j.jsbmb.2020.105720
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Article: Diminished Vitamin D Receptor Protein Levels in Crohn’s Disease Fibroblasts: Effects of Vitamin D

Nutrients. 2020 Apr. 01, v. 12, no. 4

2020

Abstract: Vitamin D (VD) deficiency has been associated to Crohn’s disease (CD) pathogenesis, and the exogenous administration of VD improves the course of the disease, but the mechanistic basis of these observations remains unknown. Vitamin D receptor (VDR) ... ...

Abstract	Vitamin D (VD) deficiency has been associated to Crohn’s disease (CD) pathogenesis, and the exogenous administration of VD improves the course of the disease, but the mechanistic basis of these observations remains unknown. Vitamin D receptor (VDR) mediates most of the biological functions of this hormone, and we aim to analyze here the expression of VDR in intestinal tissue, epithelial cells, and fibroblasts from CD patients. The effects of VD on a fibroblast wound healing assay and murine intestinal fibrosis are also analyzed. Our data show diminished VDR protein levels in surgical resections and epithelial cells from CD patients. In intestinal fibroblasts isolated from damaged tissue of CD patients, we detected enhanced migration and decreased VDR expression compared with both fibroblasts from non-damaged tissue of the same CD patient or control fibroblasts. Treatment with VD increased VDR protein levels, avoided the accelerated migration in CD fibroblasts, and prevented murine intestinal fibrosis induced by the heterotopic transplant model. In conclusion, our study demonstrates diminished VDR protein levels associated with enhanced migration in intestinal fibroblasts from damaged tissue of CD patients. In these cells, VD accumulates VDR and normalizes migration, which supports that CD patients would benefit from the VD anti-fibrotic therapeutic value that we demonstrate in a murine experimental model.
Keywords	assays ; calcitriol receptors ; epithelial cells ; fibroblasts ; fibrosis ; intestines ; mice ; models ; nutrients ; pathogenesis ; patients ; protein content ; therapeutics ; tissue repair ; vitamin D
Language	English
Dates of publication	2020-0401
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
Note	NAL-light
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu12040973
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Article ; Online: Autophagy Stimulation as a Potential Strategy Against Intestinal Fibrosis.

Cosin-Roger, Jesus / Canet, Francisco / Macias-Ceja, Dulce C / Gisbert-Ferrándiz, Laura / Ortiz-Masiá, Dolores / Esplugues, Juan V / Alós, Rafael / Navarro, Francisco / Barrachina, María D / Calatayud, Sara

Cells

2019 Volume 8, Issue 9

Abstract: We recently observed reduced autophagy in Crohn's disease patients and an anti-inflammatory effect of autophagy stimulation in murine colitis, but both anti- and pro-fibrotic effects are associated with autophagy stimulation in different tissues, and ... ...

Abstract	We recently observed reduced autophagy in Crohn's disease patients and an anti-inflammatory effect of autophagy stimulation in murine colitis, but both anti- and pro-fibrotic effects are associated with autophagy stimulation in different tissues, and fibrosis is a frequent complication of Crohn's disease. Thus, we analyzed the effects of pharmacological modulation of autophagy in a murine model of intestinal fibrosis and detected that autophagy inhibition aggravates, while autophagy stimulation prevents, fibrosis. These effects are associated with changes in inflammation and in collagen degradation in primary fibroblasts. Thus, pharmacological stimulation of autophagy may be useful against intestinal fibrosis.
MeSH term(s)	Animals ; Autophagy/drug effects ; Collagen/metabolism ; Crohn Disease/complications ; Disease Models, Animal ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Fibrosis/drug therapy ; Immunosuppressive Agents/pharmacology ; Inflammation/drug therapy ; Inflammation/immunology ; Intestines/pathology ; Mice ; Mice, Inbred C57BL ; Sirolimus/pharmacology
Chemical Substances	Immunosuppressive Agents ; Collagen (9007-34-5) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2019-09-13
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8091078
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Article ; Online: WNT2b Activates Epithelial-mesenchymal Transition Through FZD4: Relevance in Penetrating Crohn´s Disease.

Ortiz-Masià, Dolores / Salvador, Pedro / Macias-Ceja, Dulce C / Gisbert-Ferrándiz, Laura / Esplugues, Juan V / Manyé, Josep / Alós, Rafael / Navarro-Vicente, Francisco / Mamie, Céline / Scharl, Michael / Cosin-Roger, Jesus / Calatayud, Sara / Barrachina, María D

Journal of Crohn's & colitis

2019 Volume 14, Issue 2, Page(s) 230–239

Abstract: Background and aims: Epithelial-mesenchymal transition [EMT] has been related to fibrosis and fistula formation, common complications associated with Crohn´s disease [CD]. The WNT signalling pathway mediates EMT, and specific WNT/FZD interactions have ... ...

Abstract	Background and aims: Epithelial-mesenchymal transition [EMT] has been related to fibrosis and fistula formation, common complications associated with Crohn´s disease [CD]. The WNT signalling pathway mediates EMT, and specific WNT/FZD interactions have been related to the activation of this process in several diseases. We aim to analyse the relevance of EMT and WNT ligands and receptors in the penetrating behaviour of CD. Methods: Intestinal surgical resections were obtained from control and CD patients with a stenotic or penetrating behaviour. Fibrosis was determined by the histological analysis of collagen deposition and EMT by confocal microscopy. The expression of WNT ligands, inhibitors, and FZD receptors was analysed by RT-PCR, WB, IH, and IF studies. The effects of WNT2b and the role of FZD4 in EMT were analysed in HT29 epithelial cells. Results: Fibrosis and expression of EMT markers were detected in samples from CD patients irrespective of the clinical behaviour. However, an increased colocalisation of E-CADHERIN and VIMENTIN, an increased number of cells expressing WNT2b, and a higher expression of FZD4 and WNT2b/FZD4 interaction, were detected in intestinal tissue from the penetrating compared with the stenotic CD behaviour. WNT2b induced EMT in HT29 cells through FZD4 activation. Conclusions: An increased EMT, associated with increased WNT2b/FZD4 interaction, was detected in intestinal tissue from CD patients with a penetrating behaviour. WNT2b, through FZD4 activation, induces EMT in vitro which points to a novel pharmacological target to prevent intestinal penetrating complications of CD.
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Blotting, Western ; Colon/metabolism ; Colon/pathology ; Crohn Disease/metabolism ; Crohn Disease/pathology ; Epithelial-Mesenchymal Transition ; Female ; Fibrosis ; Frizzled Receptors/metabolism ; Glycoproteins/metabolism ; HT29 Cells ; Humans ; Immunoprecipitation ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/pathology ; Male ; Middle Aged ; Real-Time Polymerase Chain Reaction ; Wnt Proteins/metabolism ; Wnt Signaling Pathway ; Young Adult
Chemical Substances	FZD4 protein, human ; Frizzled Receptors ; Glycoproteins ; WNT2B protein, human ; Wnt Proteins
Language	English
Publishing date	2019-07-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2390120-2
ISSN	1876-4479 ; 1873-9946
ISSN (online)	1876-4479
ISSN	1873-9946
DOI	10.1093/ecco-jcc/jjz134
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Article ; Online: Stimulation of autophagy prevents intestinal mucosal inflammation and ameliorates murine colitis.

Macias-Ceja, Dulce C / Cosín-Roger, Jesús / Ortiz-Masiá, Dolores / Salvador, Pedro / Hernández, Carlos / Esplugues, Juan V / Calatayud, Sara / Barrachina, María D

British journal of pharmacology

2017 Volume 174, Issue 15, Page(s) 2501–2511

Abstract: Background and purpose: Defective autophagy contributes to the pathogenesis of inflammatory disorders such as inflammatory bowel disease and there are interactions between autophagy and inflammation. Here we have analysed the effects of autophagy ... ...

Abstract	Background and purpose: Defective autophagy contributes to the pathogenesis of inflammatory disorders such as inflammatory bowel disease and there are interactions between autophagy and inflammation. Here we have analysed the effects of autophagy stimulators on murine colitis. Experimental approach: Mice were treated with intrarectal administration of 2,4,6-trinitrobenzenesulfonic acid (TNBS) (3.5 mg·20 g Key results: Impaired autophagy associated with body weight loss and intestinal damage was detected in the mucosa of TNBS-treated mice. Administration of trehalose, rapamycin or betanin prevented the impaired autophagic flux induced by TNBS and decreased mucosal protein levels of BCL10, p-IκBα and NFκB-p65 and the expression of pro-inflammatory cytokines and M1 macrophage markers. Blockade of autophagosome formation by treatment with 3MA, prevented the reduction in protein levels of p62, BCL10, p-IκBα and NFκB-p65 induced by betanin in TNBS-treated mice and weakened the protective effects of betanin on murine colitis. Conclusions and implications: Pharmacological stimulation of mucosal autophagy reduced intestinal inflammation and improved murine colitis.
MeSH term(s)	Administration, Rectal ; Animals ; Autophagy/drug effects ; Betacyanins/administration & dosage ; Betacyanins/pharmacology ; Colitis/chemically induced ; Colitis/drug therapy ; Colitis/pathology ; Female ; Inflammation/drug therapy ; Inflammation/metabolism ; Injections, Intraperitoneal ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Sirolimus/administration & dosage ; Sirolimus/pharmacology ; Trehalose/administration & dosage ; Trehalose/pharmacology ; Trinitrobenzenesulfonic Acid/administration & dosage
Chemical Substances	Betacyanins ; betanin (5YJC992ZP6) ; Trinitrobenzenesulfonic Acid (8T3HQG2ZC4) ; Trehalose (B8WCK70T7I) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2017-06-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.13860
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