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Official Journal of the Italian Society of Angiology and Vascular Pathology
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,752
Online ISSN 1827-1618
Lia X. 1, 2, Gong J. 2, Meng H. 2, Ji L. 2, Chen L. 2, Yang M. 2, Liu B. 2, Geng L. 2, Kong J. 1
1 Department of Geriatric, the first hospital of Ji Lin University, Changchun, Jilin province, China;
2 Department of Cardiology, Changchun Central Hospital, Changchun, Jilin province,China
OBJECTIVE: In this study, we aimed to investigate molecular mechanisms for rhamnetin in oxidative damaged myocardial cells and provide some new treatment targets for myocardial oxidative stress injure by bioinformatic analysis.
METHODS: Two RNA libraries (control and rhamnetin exposure) from H9c2 cells were constructed and sequenced. After differentially expressed genes (DEGs) identified by NOISeq package, pathways and function analyses were conducted by KEGG and GO BP through DAVID online tool, respectively. Additionally, STRING database was used to constructed protein-protein interaction (PPI) network and MCODE was performed for module analysis.
RESULT: A total of 703 up- and 749 down- regulated genes were screened between rhamnetin and control groups. The up-regulated genes were mainly enriched in Adherens junction, Notch signaling pathway and Focal adhesion pathways as well as biological and cellular regulating processes, while the down-regulated genes were mainly enriched in pathways and processes related with oxidative phosphorylation, diseases cell cycle and metabolism. PPI network was constructed with 609 nodes and the top ten nodes were selected with high degrees. Additionally, two modules were obtained with score > 6.
CONCLUSION: Our study supplied the theoretical basis for uncovering the molecular mechanism of rhamnetin and potential therapeutic targets for myocardial diseases.