快速检索
年期检索
摘要： Abstract Epicatechin gallate (ECG) is one of the polyphenolic compounds and has attracted much attention due to its various bioactivities. In this study, the neuroprotective effect of ECG against H2O2-induced oxidative injury in PC12 cells as well as the possible mechanisms were investigated. Cell viability was determined by MTT assay. The differentially expressed genes (DEGs), GO enrichment, and KEGG enrichment were analyzed to explore the mechanism of ECG against H2O2-induced oxidative injury by using the RNA-seq method. Finally, the change in the cell cycle was analyzed by flow cytometry. H2O2 (400-1200 μ mol/L) inhibited the cell viability in a concentration-dependent manner. ECG (6-150 μmol/L) eff ectively attenuated the H2O2-induced decrease in cell viability. RNA-seq analysis showed that ECG regulated 1 058 coexpressed DEGs. GO enrichment analysis showed that the cellular component was the dominant group after ECG treatment. KEGG analysis showed that the cell cycle, fanconi anemia pathway, and homologous recombination were the important pathways for ECG in improving H2O2-induced oxidative injury and 28 coexpressed DEGs in the cell cycle pathway were summarized. Finally, cell cycle analysis also proved that ECG improved H2O2-induced cell cycle arrest in the G2/M phase. Our present study demonstrated that ECG attenuated H2O2-induced neurologic oxidative damage by multiple modulatory mechanisms at the molecular transcription level. These fi ndings provide new insights for further study of the molecular mechanism of the neuroprotection of ECG.
