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Published on: September 9, 2021
Effects of Gypenoside XLIX on fatty liver cell gene expression in vitro: a genome-wide analysis
Fengming Liu1, Qiu Wei2, Yidan Liang2
1Department of Critical Care Medicine, The First People's Hospital of Nanning Nanning 530022, Guangxi, China.
Objective:
To perform Genome-wide analysis of Gypenoside XLIX (Gyp-XLIX) in the treatment of fatty liver cells.
Methods:
The gene profiles of 3 normal liver cells, 3 fatty liver cells, and 3 fatty liver cells treated with Gyp-XLIX were detected by high-throughput sequencing to identify the differentially expressed genes (DEGs) in fatty liver treated by Gyp-XLIX. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were used to explore the biological functions of DEGs. By constructing lncRNA-mRNA co-expression network of DEGs, network node genes were mined. Possible target genes of differentially expressed lncRNA were predicted by cis regulation.
Results:
782 DEGs were screened out; that is, 172 genes were highly expressed in fatty liver cells, and the expression decreased to the level of normal liver cells after Gyp-XLIX treatment; 610 genes were under expressed in fatty liver cells, and the expression increased to the level of normal liver cells after Gyp-XLIX treatment. Functional analysis of KEGG and GO showed that DEGs process DNA-binding transcription factor activity and ion transmembrane transporter activity in the plasma membrane region. This mediates glycerophospholipid metabolism, bile secretion, fatty acid degradation and other signaling pathways. lncRNA analysis showed that the expression of 16 lncRNAs was low in fatty liver cells, and the expression was increased to the level of normal liver cells after Gyp-XLIX treatment. Target gene prediction showed that 16 differentially expressed lncRNAs had cis potential to regulate target genes, among which lncRNA RPARP-AS1 had a high degree of relationship with other genes. lncRNA-mRNA co-expression network results showed that lncRNA RPARP-AS1 may acted on NFKB2.
Conclusion:
LncRNA was differentially expressed in fatty liver cells and Gyp-XLIX treated fatty liver cells, and lncRNA RPARP-AS1 may be a regulatory gene in Gyp-XLIX treated fatty liver.
Insights
Gypenoside XLIX (Gyp-XLIX) treatment altered gene expression in fatty liver cells, impacting pathways like lipid metabolism. Long non-coding RNA RPARP-AS1 showed differential expression and may regulate NFKB2 in Gyp-XLIX treated fatty liver.
Area of Science:
- Molecular Biology
- Genomics
- Biochemistry
Background:
- Fatty liver disease is characterized by abnormal lipid accumulation in hepatocytes.
- Understanding the molecular mechanisms underlying fatty liver is crucial for developing effective treatments.
- Gypenoside XLIX (Gyp-XLIX) is a compound with potential therapeutic properties.
Purpose of the Study:
- To conduct a genome-wide analysis of Gypenoside XLIX (Gyp-XLIX) effects on fatty liver cells.
- To identify differentially expressed genes (DEGs) and long non-coding RNAs (lncRNAs) in response to Gyp-XLIX treatment.
- To elucidate the molecular pathways and regulatory networks involved in Gyp-XLIX's action on fatty liver.
Main Methods:
- High-throughput sequencing was employed to analyze gene profiles of normal, fatty, and Gyp-XLIX treated fatty liver cells.
- Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed on DEGs.
- lncRNA-mRNA co-expression networks were constructed, and cis-regulatory interactions were predicted.
Main Results:
- A total of 782 DEGs were identified, with 172 upregulated and 610 downregulated in fatty liver cells compared to normal cells, and their expression normalized after Gyp-XLIX treatment.
- Functional analysis revealed that DEGs are involved in DNA-binding transcription factor activity, ion transmembrane transport, glycerophospholipid metabolism, bile secretion, and fatty acid degradation.
- Sixteen lncRNAs showed differential expression, with lncRNA RPARP-AS1 identified as a key regulatory molecule potentially targeting NFKB2 via cis-regulation.
Conclusions:
- Gyp-XLIX treatment significantly alters gene expression profiles in fatty liver cells.
- lncRNA RPARP-AS1 is differentially expressed in fatty liver and may play a regulatory role in Gyp-XLIX's therapeutic effects.
- The findings provide insights into the molecular mechanisms of Gyp-XLIX in treating fatty liver disease.
