Transcriptomic analysis provides insights into the molecular mechanisms of epigallocatechin-3-gallate to attenuate schistosomiasis hepatic fibrosis in mice

Jinmei Feng, Fahu Yuan, Stephen Hsu, Wenjian Song

Research output: Contribution to journalArticle

Abstract

Epigallocatechin-3-gallate (EGCG) was shown to possess anti-inflammatory, anti-infection, and anti-fibrotic effects. Our previous study showed EGCG could attenuate Schistosoma japonicum hepatic fibrosis, however, its underlying molecular mechanisms are still elusive. In this work, RNA-sequencing (RNA-seq) and bioinformatics analyses were used to detect the gene expression alterations in S. japonicum hepatic fibrosis mouse model following EGCG treatment. Our results showed 106 common differentially expressed genes (DEGs) were upregulated in EGCG_LF_vs._Mod_LF (EGCG treatment group relative to S. japonicum infected model group) and downregulated in Mod_LF_vs._Nor_LF (model group relative to normal group), and they are enriched in cytochrome and metabolic genes involving in the metabolism pathways, implying EGCG could improve the S. japonicum egg induced hepatic injury and recover the metabolic functions of the liver. The 410 common DEGs, downregulated in EGCG_LF_vs._Mod_LF and upregulated in Mod_LF_vs._Nor_LF, are associated primarily with inflammation and immunology. Among them, proinflammatory cytokines, chemokines to activate the hepatic stellate cells (HSCs), profibrotic genes, and extracellular matrix (ECM) production and accumulation genes, together with part components of TLR2 and NF-κB signaling pathways, were upregulated in Mod_LF_vs._Nor_LF and downregulated in EGCG_LF_vs._Mod_LF. These results indicate that EGCG treatment could ameliorate S. japonicum egg induced hepatic fibrosis progression via inhibiting the HSCs activation and reducing ECM production and accumulation, which may in part result from suppressing the TLR2 and NF-κB signaling pathways. Our results reveal the molecular mechanisms of EGCG to be used as a potential drug to regress S. japonicum egg induced hepatic fibrosis.

Original languageEnglish (US)
Pages (from-to)314-324
Number of pages11
JournalInternational Journal of Agriculture and Biology
Volume21
Issue number2
DOIs
StatePublished - Jan 1 2019

Fingerprint

schistosomiasis
liver cirrhosis
epigallocatechin
Schistosomiasis
transcriptomics
Schistosoma japonicum
Fibrosis
Liver
mice
Ovum
Hepatic Stellate Cells
Down-Regulation
Genes
genes
extracellular matrix
liver
Extracellular Matrix
parts and components
epigallocatechin gallate
RNA Sequence Analysis

Keywords

  • EGCG
  • Hepatic fibrosis
  • Mechanism
  • RNA-Seq
  • Schistosoma japonicum

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)

Cite this

@article{228c4b4878984b59b8c81a341ee6f31b,
title = "Transcriptomic analysis provides insights into the molecular mechanisms of epigallocatechin-3-gallate to attenuate schistosomiasis hepatic fibrosis in mice",
abstract = "Epigallocatechin-3-gallate (EGCG) was shown to possess anti-inflammatory, anti-infection, and anti-fibrotic effects. Our previous study showed EGCG could attenuate Schistosoma japonicum hepatic fibrosis, however, its underlying molecular mechanisms are still elusive. In this work, RNA-sequencing (RNA-seq) and bioinformatics analyses were used to detect the gene expression alterations in S. japonicum hepatic fibrosis mouse model following EGCG treatment. Our results showed 106 common differentially expressed genes (DEGs) were upregulated in EGCG_LF_vs._Mod_LF (EGCG treatment group relative to S. japonicum infected model group) and downregulated in Mod_LF_vs._Nor_LF (model group relative to normal group), and they are enriched in cytochrome and metabolic genes involving in the metabolism pathways, implying EGCG could improve the S. japonicum egg induced hepatic injury and recover the metabolic functions of the liver. The 410 common DEGs, downregulated in EGCG_LF_vs._Mod_LF and upregulated in Mod_LF_vs._Nor_LF, are associated primarily with inflammation and immunology. Among them, proinflammatory cytokines, chemokines to activate the hepatic stellate cells (HSCs), profibrotic genes, and extracellular matrix (ECM) production and accumulation genes, together with part components of TLR2 and NF-κB signaling pathways, were upregulated in Mod_LF_vs._Nor_LF and downregulated in EGCG_LF_vs._Mod_LF. These results indicate that EGCG treatment could ameliorate S. japonicum egg induced hepatic fibrosis progression via inhibiting the HSCs activation and reducing ECM production and accumulation, which may in part result from suppressing the TLR2 and NF-κB signaling pathways. Our results reveal the molecular mechanisms of EGCG to be used as a potential drug to regress S. japonicum egg induced hepatic fibrosis.",
keywords = "EGCG, Hepatic fibrosis, Mechanism, RNA-Seq, Schistosoma japonicum",
author = "Jinmei Feng and Fahu Yuan and Stephen Hsu and Wenjian Song",
year = "2019",
month = "1",
day = "1",
doi = "10.17957/IJAB/15.0896",
language = "English (US)",
volume = "21",
pages = "314--324",
journal = "International Journal of Agriculture and Biology",
issn = "1560-8530",
publisher = "Friends Science Publishers",
number = "2",

}

TY - JOUR

T1 - Transcriptomic analysis provides insights into the molecular mechanisms of epigallocatechin-3-gallate to attenuate schistosomiasis hepatic fibrosis in mice

AU - Feng, Jinmei

AU - Yuan, Fahu

AU - Hsu, Stephen

AU - Song, Wenjian

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Epigallocatechin-3-gallate (EGCG) was shown to possess anti-inflammatory, anti-infection, and anti-fibrotic effects. Our previous study showed EGCG could attenuate Schistosoma japonicum hepatic fibrosis, however, its underlying molecular mechanisms are still elusive. In this work, RNA-sequencing (RNA-seq) and bioinformatics analyses were used to detect the gene expression alterations in S. japonicum hepatic fibrosis mouse model following EGCG treatment. Our results showed 106 common differentially expressed genes (DEGs) were upregulated in EGCG_LF_vs._Mod_LF (EGCG treatment group relative to S. japonicum infected model group) and downregulated in Mod_LF_vs._Nor_LF (model group relative to normal group), and they are enriched in cytochrome and metabolic genes involving in the metabolism pathways, implying EGCG could improve the S. japonicum egg induced hepatic injury and recover the metabolic functions of the liver. The 410 common DEGs, downregulated in EGCG_LF_vs._Mod_LF and upregulated in Mod_LF_vs._Nor_LF, are associated primarily with inflammation and immunology. Among them, proinflammatory cytokines, chemokines to activate the hepatic stellate cells (HSCs), profibrotic genes, and extracellular matrix (ECM) production and accumulation genes, together with part components of TLR2 and NF-κB signaling pathways, were upregulated in Mod_LF_vs._Nor_LF and downregulated in EGCG_LF_vs._Mod_LF. These results indicate that EGCG treatment could ameliorate S. japonicum egg induced hepatic fibrosis progression via inhibiting the HSCs activation and reducing ECM production and accumulation, which may in part result from suppressing the TLR2 and NF-κB signaling pathways. Our results reveal the molecular mechanisms of EGCG to be used as a potential drug to regress S. japonicum egg induced hepatic fibrosis.

AB - Epigallocatechin-3-gallate (EGCG) was shown to possess anti-inflammatory, anti-infection, and anti-fibrotic effects. Our previous study showed EGCG could attenuate Schistosoma japonicum hepatic fibrosis, however, its underlying molecular mechanisms are still elusive. In this work, RNA-sequencing (RNA-seq) and bioinformatics analyses were used to detect the gene expression alterations in S. japonicum hepatic fibrosis mouse model following EGCG treatment. Our results showed 106 common differentially expressed genes (DEGs) were upregulated in EGCG_LF_vs._Mod_LF (EGCG treatment group relative to S. japonicum infected model group) and downregulated in Mod_LF_vs._Nor_LF (model group relative to normal group), and they are enriched in cytochrome and metabolic genes involving in the metabolism pathways, implying EGCG could improve the S. japonicum egg induced hepatic injury and recover the metabolic functions of the liver. The 410 common DEGs, downregulated in EGCG_LF_vs._Mod_LF and upregulated in Mod_LF_vs._Nor_LF, are associated primarily with inflammation and immunology. Among them, proinflammatory cytokines, chemokines to activate the hepatic stellate cells (HSCs), profibrotic genes, and extracellular matrix (ECM) production and accumulation genes, together with part components of TLR2 and NF-κB signaling pathways, were upregulated in Mod_LF_vs._Nor_LF and downregulated in EGCG_LF_vs._Mod_LF. These results indicate that EGCG treatment could ameliorate S. japonicum egg induced hepatic fibrosis progression via inhibiting the HSCs activation and reducing ECM production and accumulation, which may in part result from suppressing the TLR2 and NF-κB signaling pathways. Our results reveal the molecular mechanisms of EGCG to be used as a potential drug to regress S. japonicum egg induced hepatic fibrosis.

KW - EGCG

KW - Hepatic fibrosis

KW - Mechanism

KW - RNA-Seq

KW - Schistosoma japonicum

UR - http://www.scopus.com/inward/record.url?scp=85060274336&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85060274336&partnerID=8YFLogxK

U2 - 10.17957/IJAB/15.0896

DO - 10.17957/IJAB/15.0896

M3 - Article

AN - SCOPUS:85060274336

VL - 21

SP - 314

EP - 324

JO - International Journal of Agriculture and Biology

JF - International Journal of Agriculture and Biology

SN - 1560-8530

IS - 2

ER -