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Article: Emodin ameliorates glucose-induced morphologic abnormalities and synthesis of transforming growth factor β1 and fibronectin by human peritoneal mesothelial cells

TitleEmodin ameliorates glucose-induced morphologic abnormalities and synthesis of transforming growth factor β1 and fibronectin by human peritoneal mesothelial cells
Authors
KeywordsEmodin
Fibronectin
Peritoneal mesothelial cells
TGFβ1
Issue Date2001
PublisherMultimed, Inc. The Journal's web site is located at http://pdiconnect.com
Citation
Peritoneal Dialysis International, 2001, v. 21 SUPPL. 3, p. S41-S47 How to Cite?
Abstract◆ Objective: Excessive synthesis and deposition of matrix proteins by peritoneal mesothelial cells can lead to structural and functional changes in the peritoneal membrane, jeopardizing the long-term efficacy of peritoneal dialysis (PD). Prolonged exposure to high glucose concentrations in PD fluid has been implicated as a major stimulus to matrix accumulation, through the induction of transforming growth factor β1 (TGFβ1). This study investigated the effect of emodin (3-methyl-1,6,8-trihydroxyanthraquinone) on TGFβ1 and fibronectin (FN) synthesis in human peritoneal mesothelial cells (HPMCs) under high glucose concentration. ◆ Design: The HPMCs were preconditioned in either 5 mmol/L or 30 mmol/L D-glucose for 2 weeks prior to the addition of emodin. Cell viability was assessed by MTT assay and lactate dehydrogenase (LDH) release. Morphology of HPMCs was studied by phase-contrast microscopy. Modulation of TGFβ1 and FN synthesis at transcription and translation were investigated by reverse transcriptase polymerase chain reaction (RT-PCR), ELISA, and Western blot analysis. ◆ Results: When cultured under 30 mmol/L D-glucose, HPMCs demonstrated increased cell volume, multinucleation, and denudation of the monolayer, as compared with cells cultured under a physiologic (5 mmol/L) glucose concentration. High glucose concentration induced TGFβ1 synthesis by HPMCs (217.17 ± 14.88 pg/mL at 5 mmol/L D-glucose vs 370.33 ± 20.67 pg/mL at 30 mmol/L D-glucose, p < 0.0001), and FN synthesis was induced at transcription and translation. Mannitol at 30 mmol/L did not affect HPMC morphology; matrix synthesis was also unaltered. Administration of emodin together with 30 mmol/L D-glucose resulted in amelioration of cell enlargement and exfoliation, and abrogation of TGFβ1 induction (370.33 ± 20.67 pg/mL for 30 mmol/L D-glucose alone vs 260.50 ± 17.89 pg/mL for 30 mmol/L D-glucose + emodin, p < 0.0001). Synthesis of FN induced by high glucose was also reduced by 40% in the presence of emodin. ◆ Conclusions: These findings provide the first evidence that emodin can ameliorate high glucose-induced matrix synthesis in HPMCs by suppression of TGFβ1. Emodin may thus be useful in preserving peritoneal integrity in PD.
Persistent Identifierhttp://hdl.handle.net/10722/162539
ISSN
2015 Impact Factor: 1.298
2015 SCImago Journal Rankings: 0.683
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYung, Sen_HK
dc.contributor.authorLiu, ZHen_HK
dc.contributor.authorLai, KNen_HK
dc.contributor.authorLi, LSen_HK
dc.contributor.authorChan, TMen_HK
dc.date.accessioned2012-09-05T05:20:54Z-
dc.date.available2012-09-05T05:20:54Z-
dc.date.issued2001en_HK
dc.identifier.citationPeritoneal Dialysis International, 2001, v. 21 SUPPL. 3, p. S41-S47en_HK
dc.identifier.issn0896-8608en_HK
dc.identifier.urihttp://hdl.handle.net/10722/162539-
dc.description.abstract◆ Objective: Excessive synthesis and deposition of matrix proteins by peritoneal mesothelial cells can lead to structural and functional changes in the peritoneal membrane, jeopardizing the long-term efficacy of peritoneal dialysis (PD). Prolonged exposure to high glucose concentrations in PD fluid has been implicated as a major stimulus to matrix accumulation, through the induction of transforming growth factor β1 (TGFβ1). This study investigated the effect of emodin (3-methyl-1,6,8-trihydroxyanthraquinone) on TGFβ1 and fibronectin (FN) synthesis in human peritoneal mesothelial cells (HPMCs) under high glucose concentration. ◆ Design: The HPMCs were preconditioned in either 5 mmol/L or 30 mmol/L D-glucose for 2 weeks prior to the addition of emodin. Cell viability was assessed by MTT assay and lactate dehydrogenase (LDH) release. Morphology of HPMCs was studied by phase-contrast microscopy. Modulation of TGFβ1 and FN synthesis at transcription and translation were investigated by reverse transcriptase polymerase chain reaction (RT-PCR), ELISA, and Western blot analysis. ◆ Results: When cultured under 30 mmol/L D-glucose, HPMCs demonstrated increased cell volume, multinucleation, and denudation of the monolayer, as compared with cells cultured under a physiologic (5 mmol/L) glucose concentration. High glucose concentration induced TGFβ1 synthesis by HPMCs (217.17 ± 14.88 pg/mL at 5 mmol/L D-glucose vs 370.33 ± 20.67 pg/mL at 30 mmol/L D-glucose, p < 0.0001), and FN synthesis was induced at transcription and translation. Mannitol at 30 mmol/L did not affect HPMC morphology; matrix synthesis was also unaltered. Administration of emodin together with 30 mmol/L D-glucose resulted in amelioration of cell enlargement and exfoliation, and abrogation of TGFβ1 induction (370.33 ± 20.67 pg/mL for 30 mmol/L D-glucose alone vs 260.50 ± 17.89 pg/mL for 30 mmol/L D-glucose + emodin, p < 0.0001). Synthesis of FN induced by high glucose was also reduced by 40% in the presence of emodin. ◆ Conclusions: These findings provide the first evidence that emodin can ameliorate high glucose-induced matrix synthesis in HPMCs by suppression of TGFβ1. Emodin may thus be useful in preserving peritoneal integrity in PD.en_HK
dc.languageengen_US
dc.publisherMultimed, Inc. The Journal's web site is located at http://pdiconnect.comen_HK
dc.relation.ispartofPeritoneal Dialysis Internationalen_HK
dc.subjectEmodinen_HK
dc.subjectFibronectinen_HK
dc.subjectPeritoneal mesothelial cellsen_HK
dc.subjectTGFβ1en_HK
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEmodin - Pharmacologyen_US
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_US
dc.subject.meshEpithelium - Metabolism - Pathologyen_US
dc.subject.meshFibronectins - Biosynthesis - Geneticsen_US
dc.subject.meshGene Expressionen_US
dc.subject.meshGlucose - Pharmacologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMannitol - Pharmacologyen_US
dc.subject.meshPeritoneal Dialysisen_US
dc.subject.meshPeritoneum - Metabolism - Pathologyen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshTransforming Growth Factor Beta - Biosynthesis - Geneticsen_US
dc.subject.meshTransforming Growth Factor Beta1en_US
dc.titleEmodin ameliorates glucose-induced morphologic abnormalities and synthesis of transforming growth factor β1 and fibronectin by human peritoneal mesothelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailYung, S: ssyyung@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailChan, TM: dtmchan@hku.hken_HK
dc.identifier.authorityYung, S=rp00455en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityChan, TM=rp00394en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.pmid11887862-
dc.identifier.scopuseid_2-s2.0-0035570745en_HK
dc.identifier.hkuros69574-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035570745&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume21en_HK
dc.identifier.issueSUPPL. 3en_HK
dc.identifier.spageS41en_HK
dc.identifier.epageS47en_HK
dc.identifier.isiWOS:000174209500007-
dc.publisher.placeCanadaen_HK
dc.identifier.scopusauthoridYung, S=22636568800en_HK
dc.identifier.scopusauthoridLiu, ZH=36063537300en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridLi, LS=7501449836en_HK
dc.identifier.scopusauthoridChan, TM=7402687700en_HK

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