α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells

Purpose Under conditions of high ambient temperatures and/or strenuous exercise, humans and animals experience considerable heat stress (HS) leading among others to intestinal epithelial damage through induction of cellular oxidative stress. The aim of this study was to characterize the effects of α...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Varasteh, Soheil [verfasserIn] Fink-Gremmels, Johanna [verfasserIn] Garssen, Johan [verfasserIn] Braber, Saskia [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	α-Lipoic acid Heat stress Intestinal integrity Oxidative stress Inflammatory response

Übergeordnetes Werk:	Enthalten in: Zeitschrift für Ernährungswissenschaft - Darmstadt : Steinkopff, 1960, 57(2017), 4 vom: 27. März, Seite 1577-1589
Übergeordnetes Werk:	volume:57 ; year:2017 ; number:4 ; day:27 ; month:03 ; pages:1577-1589

Links:	Volltext

DOI / URN:	10.1007/s00394-017-1442-y

Katalog-ID:	SPR004877667

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245	1	0	\|a α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells
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520			\|a Purpose Under conditions of high ambient temperatures and/or strenuous exercise, humans and animals experience considerable heat stress (HS) leading among others to intestinal epithelial damage through induction of cellular oxidative stress. The aim of this study was to characterize the effects of α-Lipoic Acid (ALA) on HS-induced intestinal epithelial injury using an in vitro Caco-2 cell model. Methods A confluent monolayer of Caco-2 cells was pre-incubated with ALA (24 h) prior to control (37 °C) or HS conditions (42 °C) for 6 or 24 h and the expression of heat shock protein 70 (HSP70), heat shock factor-1 (HSF1), and the antioxidant Nrf2 were investigated. Intestinal integrity was determined by measuring transepithelial resistance, paracellular permeability, junctional complex reassembly, and E-cadherin expression and localization. Furthermore, cell proliferation was measured in an epithelial wound healing assay and the expression of the inflammatory markers cyclooxygenase-2 (COX-2) and transforming growth Factor-β (TGF-β) was evaluated. Results ALA pretreatment increased the HSP70 mRNA and protein expression under HS conditions, but did not significantly modulate the HS-induced activation of HSF1. The HS-induced increase in Nrf2 gene expression as well as the Nrf2 nuclear translocation was impeded by ALA. Moreover, ALA prevented the HS-induced impairment of intestinal integrity. Cell proliferation under HS conditions was improved by ALA supplementation as demonstrated in an epithelial wound healing assay and ALA was able to affect the HS-induced inflammatory response by decreasing the COX-2 and TGF-β mRNA expression. Conclusions ALA supplementation could prevent the disruption of intestinal epithelial integrity by enhancing epithelial cell proliferation, and reducing the inflammatory response under HS conditions in an in vitro Caco-2 cell model.
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allfields	10.1007/s00394-017-1442-y doi (DE-627)SPR004877667 (SPR)s00394-017-1442-y-e DE-627 ger DE-627 rakwb eng 630 640 610 ASE 44.21 bkl Varasteh, Soheil verfasserin aut α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Under conditions of high ambient temperatures and/or strenuous exercise, humans and animals experience considerable heat stress (HS) leading among others to intestinal epithelial damage through induction of cellular oxidative stress. The aim of this study was to characterize the effects of α-Lipoic Acid (ALA) on HS-induced intestinal epithelial injury using an in vitro Caco-2 cell model. Methods A confluent monolayer of Caco-2 cells was pre-incubated with ALA (24 h) prior to control (37 °C) or HS conditions (42 °C) for 6 or 24 h and the expression of heat shock protein 70 (HSP70), heat shock factor-1 (HSF1), and the antioxidant Nrf2 were investigated. Intestinal integrity was determined by measuring transepithelial resistance, paracellular permeability, junctional complex reassembly, and E-cadherin expression and localization. Furthermore, cell proliferation was measured in an epithelial wound healing assay and the expression of the inflammatory markers cyclooxygenase-2 (COX-2) and transforming growth Factor-β (TGF-β) was evaluated. Results ALA pretreatment increased the HSP70 mRNA and protein expression under HS conditions, but did not significantly modulate the HS-induced activation of HSF1. The HS-induced increase in Nrf2 gene expression as well as the Nrf2 nuclear translocation was impeded by ALA. Moreover, ALA prevented the HS-induced impairment of intestinal integrity. Cell proliferation under HS conditions was improved by ALA supplementation as demonstrated in an epithelial wound healing assay and ALA was able to affect the HS-induced inflammatory response by decreasing the COX-2 and TGF-β mRNA expression. Conclusions ALA supplementation could prevent the disruption of intestinal epithelial integrity by enhancing epithelial cell proliferation, and reducing the inflammatory response under HS conditions in an in vitro Caco-2 cell model. α-Lipoic acid (dpeaa)DE-He213 Heat stress (dpeaa)DE-He213 Intestinal integrity (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Inflammatory response (dpeaa)DE-He213 Fink-Gremmels, Johanna verfasserin aut Garssen, Johan verfasserin aut Braber, Saskia verfasserin aut Enthalten in Zeitschrift für Ernährungswissenschaft Darmstadt : Steinkopff, 1960 57(2017), 4 vom: 27. März, Seite 1577-1589 (DE-627)461907356 (DE-600)2164295-3 1435-1293 nnns volume:57 year:2017 number:4 day:27 month:03 pages:1577-1589 https://dx.doi.org/10.1007/s00394-017-1442-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 44.21 ASE AR 57 2017 4 27 03 1577-1589
spelling	10.1007/s00394-017-1442-y doi (DE-627)SPR004877667 (SPR)s00394-017-1442-y-e DE-627 ger DE-627 rakwb eng 630 640 610 ASE 44.21 bkl Varasteh, Soheil verfasserin aut α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Under conditions of high ambient temperatures and/or strenuous exercise, humans and animals experience considerable heat stress (HS) leading among others to intestinal epithelial damage through induction of cellular oxidative stress. The aim of this study was to characterize the effects of α-Lipoic Acid (ALA) on HS-induced intestinal epithelial injury using an in vitro Caco-2 cell model. Methods A confluent monolayer of Caco-2 cells was pre-incubated with ALA (24 h) prior to control (37 °C) or HS conditions (42 °C) for 6 or 24 h and the expression of heat shock protein 70 (HSP70), heat shock factor-1 (HSF1), and the antioxidant Nrf2 were investigated. Intestinal integrity was determined by measuring transepithelial resistance, paracellular permeability, junctional complex reassembly, and E-cadherin expression and localization. Furthermore, cell proliferation was measured in an epithelial wound healing assay and the expression of the inflammatory markers cyclooxygenase-2 (COX-2) and transforming growth Factor-β (TGF-β) was evaluated. Results ALA pretreatment increased the HSP70 mRNA and protein expression under HS conditions, but did not significantly modulate the HS-induced activation of HSF1. The HS-induced increase in Nrf2 gene expression as well as the Nrf2 nuclear translocation was impeded by ALA. Moreover, ALA prevented the HS-induced impairment of intestinal integrity. Cell proliferation under HS conditions was improved by ALA supplementation as demonstrated in an epithelial wound healing assay and ALA was able to affect the HS-induced inflammatory response by decreasing the COX-2 and TGF-β mRNA expression. Conclusions ALA supplementation could prevent the disruption of intestinal epithelial integrity by enhancing epithelial cell proliferation, and reducing the inflammatory response under HS conditions in an in vitro Caco-2 cell model. α-Lipoic acid (dpeaa)DE-He213 Heat stress (dpeaa)DE-He213 Intestinal integrity (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Inflammatory response (dpeaa)DE-He213 Fink-Gremmels, Johanna verfasserin aut Garssen, Johan verfasserin aut Braber, Saskia verfasserin aut Enthalten in Zeitschrift für Ernährungswissenschaft Darmstadt : Steinkopff, 1960 57(2017), 4 vom: 27. März, Seite 1577-1589 (DE-627)461907356 (DE-600)2164295-3 1435-1293 nnns volume:57 year:2017 number:4 day:27 month:03 pages:1577-1589 https://dx.doi.org/10.1007/s00394-017-1442-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 44.21 ASE AR 57 2017 4 27 03 1577-1589
allfields_unstemmed	10.1007/s00394-017-1442-y doi (DE-627)SPR004877667 (SPR)s00394-017-1442-y-e DE-627 ger DE-627 rakwb eng 630 640 610 ASE 44.21 bkl Varasteh, Soheil verfasserin aut α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Under conditions of high ambient temperatures and/or strenuous exercise, humans and animals experience considerable heat stress (HS) leading among others to intestinal epithelial damage through induction of cellular oxidative stress. The aim of this study was to characterize the effects of α-Lipoic Acid (ALA) on HS-induced intestinal epithelial injury using an in vitro Caco-2 cell model. Methods A confluent monolayer of Caco-2 cells was pre-incubated with ALA (24 h) prior to control (37 °C) or HS conditions (42 °C) for 6 or 24 h and the expression of heat shock protein 70 (HSP70), heat shock factor-1 (HSF1), and the antioxidant Nrf2 were investigated. Intestinal integrity was determined by measuring transepithelial resistance, paracellular permeability, junctional complex reassembly, and E-cadherin expression and localization. Furthermore, cell proliferation was measured in an epithelial wound healing assay and the expression of the inflammatory markers cyclooxygenase-2 (COX-2) and transforming growth Factor-β (TGF-β) was evaluated. Results ALA pretreatment increased the HSP70 mRNA and protein expression under HS conditions, but did not significantly modulate the HS-induced activation of HSF1. The HS-induced increase in Nrf2 gene expression as well as the Nrf2 nuclear translocation was impeded by ALA. Moreover, ALA prevented the HS-induced impairment of intestinal integrity. Cell proliferation under HS conditions was improved by ALA supplementation as demonstrated in an epithelial wound healing assay and ALA was able to affect the HS-induced inflammatory response by decreasing the COX-2 and TGF-β mRNA expression. Conclusions ALA supplementation could prevent the disruption of intestinal epithelial integrity by enhancing epithelial cell proliferation, and reducing the inflammatory response under HS conditions in an in vitro Caco-2 cell model. α-Lipoic acid (dpeaa)DE-He213 Heat stress (dpeaa)DE-He213 Intestinal integrity (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Inflammatory response (dpeaa)DE-He213 Fink-Gremmels, Johanna verfasserin aut Garssen, Johan verfasserin aut Braber, Saskia verfasserin aut Enthalten in Zeitschrift für Ernährungswissenschaft Darmstadt : Steinkopff, 1960 57(2017), 4 vom: 27. März, Seite 1577-1589 (DE-627)461907356 (DE-600)2164295-3 1435-1293 nnns volume:57 year:2017 number:4 day:27 month:03 pages:1577-1589 https://dx.doi.org/10.1007/s00394-017-1442-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 44.21 ASE AR 57 2017 4 27 03 1577-1589
allfieldsGer	10.1007/s00394-017-1442-y doi (DE-627)SPR004877667 (SPR)s00394-017-1442-y-e DE-627 ger DE-627 rakwb eng 630 640 610 ASE 44.21 bkl Varasteh, Soheil verfasserin aut α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Under conditions of high ambient temperatures and/or strenuous exercise, humans and animals experience considerable heat stress (HS) leading among others to intestinal epithelial damage through induction of cellular oxidative stress. The aim of this study was to characterize the effects of α-Lipoic Acid (ALA) on HS-induced intestinal epithelial injury using an in vitro Caco-2 cell model. Methods A confluent monolayer of Caco-2 cells was pre-incubated with ALA (24 h) prior to control (37 °C) or HS conditions (42 °C) for 6 or 24 h and the expression of heat shock protein 70 (HSP70), heat shock factor-1 (HSF1), and the antioxidant Nrf2 were investigated. Intestinal integrity was determined by measuring transepithelial resistance, paracellular permeability, junctional complex reassembly, and E-cadherin expression and localization. Furthermore, cell proliferation was measured in an epithelial wound healing assay and the expression of the inflammatory markers cyclooxygenase-2 (COX-2) and transforming growth Factor-β (TGF-β) was evaluated. Results ALA pretreatment increased the HSP70 mRNA and protein expression under HS conditions, but did not significantly modulate the HS-induced activation of HSF1. The HS-induced increase in Nrf2 gene expression as well as the Nrf2 nuclear translocation was impeded by ALA. Moreover, ALA prevented the HS-induced impairment of intestinal integrity. Cell proliferation under HS conditions was improved by ALA supplementation as demonstrated in an epithelial wound healing assay and ALA was able to affect the HS-induced inflammatory response by decreasing the COX-2 and TGF-β mRNA expression. Conclusions ALA supplementation could prevent the disruption of intestinal epithelial integrity by enhancing epithelial cell proliferation, and reducing the inflammatory response under HS conditions in an in vitro Caco-2 cell model. α-Lipoic acid (dpeaa)DE-He213 Heat stress (dpeaa)DE-He213 Intestinal integrity (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Inflammatory response (dpeaa)DE-He213 Fink-Gremmels, Johanna verfasserin aut Garssen, Johan verfasserin aut Braber, Saskia verfasserin aut Enthalten in Zeitschrift für Ernährungswissenschaft Darmstadt : Steinkopff, 1960 57(2017), 4 vom: 27. März, Seite 1577-1589 (DE-627)461907356 (DE-600)2164295-3 1435-1293 nnns volume:57 year:2017 number:4 day:27 month:03 pages:1577-1589 https://dx.doi.org/10.1007/s00394-017-1442-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 44.21 ASE AR 57 2017 4 27 03 1577-1589
allfieldsSound	10.1007/s00394-017-1442-y doi (DE-627)SPR004877667 (SPR)s00394-017-1442-y-e DE-627 ger DE-627 rakwb eng 630 640 610 ASE 44.21 bkl Varasteh, Soheil verfasserin aut α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Under conditions of high ambient temperatures and/or strenuous exercise, humans and animals experience considerable heat stress (HS) leading among others to intestinal epithelial damage through induction of cellular oxidative stress. The aim of this study was to characterize the effects of α-Lipoic Acid (ALA) on HS-induced intestinal epithelial injury using an in vitro Caco-2 cell model. Methods A confluent monolayer of Caco-2 cells was pre-incubated with ALA (24 h) prior to control (37 °C) or HS conditions (42 °C) for 6 or 24 h and the expression of heat shock protein 70 (HSP70), heat shock factor-1 (HSF1), and the antioxidant Nrf2 were investigated. Intestinal integrity was determined by measuring transepithelial resistance, paracellular permeability, junctional complex reassembly, and E-cadherin expression and localization. Furthermore, cell proliferation was measured in an epithelial wound healing assay and the expression of the inflammatory markers cyclooxygenase-2 (COX-2) and transforming growth Factor-β (TGF-β) was evaluated. Results ALA pretreatment increased the HSP70 mRNA and protein expression under HS conditions, but did not significantly modulate the HS-induced activation of HSF1. The HS-induced increase in Nrf2 gene expression as well as the Nrf2 nuclear translocation was impeded by ALA. Moreover, ALA prevented the HS-induced impairment of intestinal integrity. Cell proliferation under HS conditions was improved by ALA supplementation as demonstrated in an epithelial wound healing assay and ALA was able to affect the HS-induced inflammatory response by decreasing the COX-2 and TGF-β mRNA expression. Conclusions ALA supplementation could prevent the disruption of intestinal epithelial integrity by enhancing epithelial cell proliferation, and reducing the inflammatory response under HS conditions in an in vitro Caco-2 cell model. α-Lipoic acid (dpeaa)DE-He213 Heat stress (dpeaa)DE-He213 Intestinal integrity (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Inflammatory response (dpeaa)DE-He213 Fink-Gremmels, Johanna verfasserin aut Garssen, Johan verfasserin aut Braber, Saskia verfasserin aut Enthalten in Zeitschrift für Ernährungswissenschaft Darmstadt : Steinkopff, 1960 57(2017), 4 vom: 27. März, Seite 1577-1589 (DE-627)461907356 (DE-600)2164295-3 1435-1293 nnns volume:57 year:2017 number:4 day:27 month:03 pages:1577-1589 https://dx.doi.org/10.1007/s00394-017-1442-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 44.21 ASE AR 57 2017 4 27 03 1577-1589
language	English
source	Enthalten in Zeitschrift für Ernährungswissenschaft 57(2017), 4 vom: 27. März, Seite 1577-1589 volume:57 year:2017 number:4 day:27 month:03 pages:1577-1589
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topic_facet	α-Lipoic acid Heat stress Intestinal integrity Oxidative stress Inflammatory response
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The HS-induced increase in Nrf2 gene expression as well as the Nrf2 nuclear translocation was impeded by ALA. Moreover, ALA prevented the HS-induced impairment of intestinal integrity. Cell proliferation under HS conditions was improved by ALA supplementation as demonstrated in an epithelial wound healing assay and ALA was able to affect the HS-induced inflammatory response by decreasing the COX-2 and TGF-β mRNA expression. 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author	Varasteh, Soheil
spellingShingle	Varasteh, Soheil ddc 630 bkl 44.21 misc α-Lipoic acid misc Heat stress misc Intestinal integrity misc Oxidative stress misc Inflammatory response α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells
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topic_title	630 640 610 ASE 44.21 bkl α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells α-Lipoic acid (dpeaa)DE-He213 Heat stress (dpeaa)DE-He213 Intestinal integrity (dpeaa)DE-He213 Oxidative stress (dpeaa)DE-He213 Inflammatory response (dpeaa)DE-He213
topic	ddc 630 bkl 44.21 misc α-Lipoic acid misc Heat stress misc Intestinal integrity misc Oxidative stress misc Inflammatory response
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title	α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells
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title_full	α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells
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title_sort	α-lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in caco-2 cells
title_auth	α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells
abstract	Purpose Under conditions of high ambient temperatures and/or strenuous exercise, humans and animals experience considerable heat stress (HS) leading among others to intestinal epithelial damage through induction of cellular oxidative stress. The aim of this study was to characterize the effects of α-Lipoic Acid (ALA) on HS-induced intestinal epithelial injury using an in vitro Caco-2 cell model. Methods A confluent monolayer of Caco-2 cells was pre-incubated with ALA (24 h) prior to control (37 °C) or HS conditions (42 °C) for 6 or 24 h and the expression of heat shock protein 70 (HSP70), heat shock factor-1 (HSF1), and the antioxidant Nrf2 were investigated. Intestinal integrity was determined by measuring transepithelial resistance, paracellular permeability, junctional complex reassembly, and E-cadherin expression and localization. Furthermore, cell proliferation was measured in an epithelial wound healing assay and the expression of the inflammatory markers cyclooxygenase-2 (COX-2) and transforming growth Factor-β (TGF-β) was evaluated. Results ALA pretreatment increased the HSP70 mRNA and protein expression under HS conditions, but did not significantly modulate the HS-induced activation of HSF1. The HS-induced increase in Nrf2 gene expression as well as the Nrf2 nuclear translocation was impeded by ALA. Moreover, ALA prevented the HS-induced impairment of intestinal integrity. Cell proliferation under HS conditions was improved by ALA supplementation as demonstrated in an epithelial wound healing assay and ALA was able to affect the HS-induced inflammatory response by decreasing the COX-2 and TGF-β mRNA expression. Conclusions ALA supplementation could prevent the disruption of intestinal epithelial integrity by enhancing epithelial cell proliferation, and reducing the inflammatory response under HS conditions in an in vitro Caco-2 cell model.
abstractGer	Purpose Under conditions of high ambient temperatures and/or strenuous exercise, humans and animals experience considerable heat stress (HS) leading among others to intestinal epithelial damage through induction of cellular oxidative stress. The aim of this study was to characterize the effects of α-Lipoic Acid (ALA) on HS-induced intestinal epithelial injury using an in vitro Caco-2 cell model. Methods A confluent monolayer of Caco-2 cells was pre-incubated with ALA (24 h) prior to control (37 °C) or HS conditions (42 °C) for 6 or 24 h and the expression of heat shock protein 70 (HSP70), heat shock factor-1 (HSF1), and the antioxidant Nrf2 were investigated. Intestinal integrity was determined by measuring transepithelial resistance, paracellular permeability, junctional complex reassembly, and E-cadherin expression and localization. Furthermore, cell proliferation was measured in an epithelial wound healing assay and the expression of the inflammatory markers cyclooxygenase-2 (COX-2) and transforming growth Factor-β (TGF-β) was evaluated. Results ALA pretreatment increased the HSP70 mRNA and protein expression under HS conditions, but did not significantly modulate the HS-induced activation of HSF1. The HS-induced increase in Nrf2 gene expression as well as the Nrf2 nuclear translocation was impeded by ALA. Moreover, ALA prevented the HS-induced impairment of intestinal integrity. Cell proliferation under HS conditions was improved by ALA supplementation as demonstrated in an epithelial wound healing assay and ALA was able to affect the HS-induced inflammatory response by decreasing the COX-2 and TGF-β mRNA expression. Conclusions ALA supplementation could prevent the disruption of intestinal epithelial integrity by enhancing epithelial cell proliferation, and reducing the inflammatory response under HS conditions in an in vitro Caco-2 cell model.
abstract_unstemmed	Purpose Under conditions of high ambient temperatures and/or strenuous exercise, humans and animals experience considerable heat stress (HS) leading among others to intestinal epithelial damage through induction of cellular oxidative stress. The aim of this study was to characterize the effects of α-Lipoic Acid (ALA) on HS-induced intestinal epithelial injury using an in vitro Caco-2 cell model. Methods A confluent monolayer of Caco-2 cells was pre-incubated with ALA (24 h) prior to control (37 °C) or HS conditions (42 °C) for 6 or 24 h and the expression of heat shock protein 70 (HSP70), heat shock factor-1 (HSF1), and the antioxidant Nrf2 were investigated. Intestinal integrity was determined by measuring transepithelial resistance, paracellular permeability, junctional complex reassembly, and E-cadherin expression and localization. Furthermore, cell proliferation was measured in an epithelial wound healing assay and the expression of the inflammatory markers cyclooxygenase-2 (COX-2) and transforming growth Factor-β (TGF-β) was evaluated. Results ALA pretreatment increased the HSP70 mRNA and protein expression under HS conditions, but did not significantly modulate the HS-induced activation of HSF1. The HS-induced increase in Nrf2 gene expression as well as the Nrf2 nuclear translocation was impeded by ALA. Moreover, ALA prevented the HS-induced impairment of intestinal integrity. Cell proliferation under HS conditions was improved by ALA supplementation as demonstrated in an epithelial wound healing assay and ALA was able to affect the HS-induced inflammatory response by decreasing the COX-2 and TGF-β mRNA expression. Conclusions ALA supplementation could prevent the disruption of intestinal epithelial integrity by enhancing epithelial cell proliferation, and reducing the inflammatory response under HS conditions in an in vitro Caco-2 cell model.
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title_short	α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells
url	https://dx.doi.org/10.1007/s00394-017-1442-y
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author2	Fink-Gremmels, Johanna Garssen, Johan Braber, Saskia
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The HS-induced increase in Nrf2 gene expression as well as the Nrf2 nuclear translocation was impeded by ALA. Moreover, ALA prevented the HS-induced impairment of intestinal integrity. Cell proliferation under HS conditions was improved by ALA supplementation as demonstrated in an epithelial wound healing assay and ALA was able to affect the HS-induced inflammatory response by decreasing the COX-2 and TGF-β mRNA expression. 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α-Lipoic acid prevents the intestinal epithelial monolayer damage under heat stress conditions: model experiments in Caco-2 cells

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