Cargando…

Protective effect of cornel iridoid glycoside in D-galactosamine/tumor necrosis factor-α-injured L02 hepatocytes and its mechanism

AIM: The aim was to determine the action mode of cornel iridoid glycoside (CIG) from Fructus corni on hepatoprotective activities, the effects of CIG on human hepatocyte cell line (L02) injured by D-galactosamine (GalN) and tumor necrosis factor-α (TNF-α) were examined. MATERIALS AND METHODS: The pe...

Descripción completa

Detalles Bibliográficos
Autores principales: Jiang, Zequn, Ma, Yanxia, Zhou, Lihua, Jiang, Haiying, Wang, Mingyan, Zhan, Xiuqin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGEYA 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4576803/
https://www.ncbi.nlm.nih.gov/pubmed/26401374
http://dx.doi.org/10.5455/jice.20140916011549
_version_ 1782390903312220160
author Jiang, Zequn
Ma, Yanxia
Zhou, Lihua
Jiang, Haiying
Wang, Mingyan
Zhan, Xiuqin
author_facet Jiang, Zequn
Ma, Yanxia
Zhou, Lihua
Jiang, Haiying
Wang, Mingyan
Zhan, Xiuqin
author_sort Jiang, Zequn
collection PubMed
description AIM: The aim was to determine the action mode of cornel iridoid glycoside (CIG) from Fructus corni on hepatoprotective activities, the effects of CIG on human hepatocyte cell line (L02) injured by D-galactosamine (GalN) and tumor necrosis factor-α (TNF-α) were examined. MATERIALS AND METHODS: The percentage of cell viability was evaluated by cell counting kit-8 assay. Apoptosis was detected by flow cytometric analysis in human L02 hepatocytes. The expression levels of activating transcription factor-4 (ATF4), and C/EBP homologous protein (CHOP) were detected by western-blot analysis. In addition, the activity of caspase-3 was tested by enzyme-linked immunosorbent assay. RESULTS: The results showed that CIG caused a significant increase in the viability of L02 cells injured by GalN/TNF-α, in accordance with a dose-dependent decrease of apoptotic cell death confirmed by flow cytometric analysis. Based on western blot and colorimetric assay, we found that GalN/TNF-α induced increased expression of ATF4, CHOP, and activation of caspase-3 while CIG pre-treatment had a dose-dependent suppression on them in this cell model. CONCLUSION: Overall, these findings demonstrate that CIG can effectively protect L02 hepatocytes against apoptosis induced by GalN/TNF-α, suggesting that it is a possible candidate target for liver disease therapy.
format Online
Article
Text
id pubmed-4576803
institution National Center for Biotechnology Information
language English
publishDate 2014
publisher SAGEYA
record_format MEDLINE/PubMed
spelling pubmed-45768032015-09-23 Protective effect of cornel iridoid glycoside in D-galactosamine/tumor necrosis factor-α-injured L02 hepatocytes and its mechanism Jiang, Zequn Ma, Yanxia Zhou, Lihua Jiang, Haiying Wang, Mingyan Zhan, Xiuqin J Intercult Ethnopharmacol Original Research AIM: The aim was to determine the action mode of cornel iridoid glycoside (CIG) from Fructus corni on hepatoprotective activities, the effects of CIG on human hepatocyte cell line (L02) injured by D-galactosamine (GalN) and tumor necrosis factor-α (TNF-α) were examined. MATERIALS AND METHODS: The percentage of cell viability was evaluated by cell counting kit-8 assay. Apoptosis was detected by flow cytometric analysis in human L02 hepatocytes. The expression levels of activating transcription factor-4 (ATF4), and C/EBP homologous protein (CHOP) were detected by western-blot analysis. In addition, the activity of caspase-3 was tested by enzyme-linked immunosorbent assay. RESULTS: The results showed that CIG caused a significant increase in the viability of L02 cells injured by GalN/TNF-α, in accordance with a dose-dependent decrease of apoptotic cell death confirmed by flow cytometric analysis. Based on western blot and colorimetric assay, we found that GalN/TNF-α induced increased expression of ATF4, CHOP, and activation of caspase-3 while CIG pre-treatment had a dose-dependent suppression on them in this cell model. CONCLUSION: Overall, these findings demonstrate that CIG can effectively protect L02 hepatocytes against apoptosis induced by GalN/TNF-α, suggesting that it is a possible candidate target for liver disease therapy. SAGEYA 2014-09-27 /pmc/articles/PMC4576803/ /pubmed/26401374 http://dx.doi.org/10.5455/jice.20140916011549 Text en Copyright: © SAGEYA http://creativecommons.org/licenses/by-nc/3.0/ This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, noncommercial use, distribution and reproduction in any medium, provided the work is properly cited.
spellingShingle Original Research
Jiang, Zequn
Ma, Yanxia
Zhou, Lihua
Jiang, Haiying
Wang, Mingyan
Zhan, Xiuqin
Protective effect of cornel iridoid glycoside in D-galactosamine/tumor necrosis factor-α-injured L02 hepatocytes and its mechanism
title Protective effect of cornel iridoid glycoside in D-galactosamine/tumor necrosis factor-α-injured L02 hepatocytes and its mechanism
title_full Protective effect of cornel iridoid glycoside in D-galactosamine/tumor necrosis factor-α-injured L02 hepatocytes and its mechanism
title_fullStr Protective effect of cornel iridoid glycoside in D-galactosamine/tumor necrosis factor-α-injured L02 hepatocytes and its mechanism
title_full_unstemmed Protective effect of cornel iridoid glycoside in D-galactosamine/tumor necrosis factor-α-injured L02 hepatocytes and its mechanism
title_short Protective effect of cornel iridoid glycoside in D-galactosamine/tumor necrosis factor-α-injured L02 hepatocytes and its mechanism
title_sort protective effect of cornel iridoid glycoside in d-galactosamine/tumor necrosis factor-α-injured l02 hepatocytes and its mechanism
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4576803/
https://www.ncbi.nlm.nih.gov/pubmed/26401374
http://dx.doi.org/10.5455/jice.20140916011549
work_keys_str_mv AT jiangzequn protectiveeffectofcorneliridoidglycosideindgalactosaminetumornecrosisfactorainjuredl02hepatocytesanditsmechanism
AT mayanxia protectiveeffectofcorneliridoidglycosideindgalactosaminetumornecrosisfactorainjuredl02hepatocytesanditsmechanism
AT zhoulihua protectiveeffectofcorneliridoidglycosideindgalactosaminetumornecrosisfactorainjuredl02hepatocytesanditsmechanism
AT jianghaiying protectiveeffectofcorneliridoidglycosideindgalactosaminetumornecrosisfactorainjuredl02hepatocytesanditsmechanism
AT wangmingyan protectiveeffectofcorneliridoidglycosideindgalactosaminetumornecrosisfactorainjuredl02hepatocytesanditsmechanism
AT zhanxiuqin protectiveeffectofcorneliridoidglycosideindgalactosaminetumornecrosisfactorainjuredl02hepatocytesanditsmechanism