Epicatechin gallate(ECG)is one of the polyphenolic compounds and has attracted much attention due to its various bioactivities.In this study,the neuroprotective eff ect of ECG against H_(2)O_(2)-induced oxidative inju...Epicatechin gallate(ECG)is one of the polyphenolic compounds and has attracted much attention due to its various bioactivities.In this study,the neuroprotective eff ect of ECG against H_(2)O_(2)-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 H_(2)O_(2)-induced oxidative injury by using the RNA-seq method.Finally,the change in the cell cycle was analyzed by fl ow cytometry.H_(2)O_(2)(400-1200μmol/L)inhibited the cell viability in a concentration-dependent manner.ECG(6-150μmol/L)eff ectively attenuated the H_(2)O_(2)-induced decrease in cell viability.RNA-seq analysis showed that ECG regulated 1058 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 H_(2)O_(2)-induced oxidative injury and 28 coexpressed DEGs in the cell cycle pathway were summarized.Finally,cell cycle analysis also proved that ECG improved H_(2)O_(2)-induced cell cycle arrest in the G2/M phase.Our present study demonstrated that ECG attenuated H_(2)O_(2)-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.展开更多
基金This work was supported by College Students Innovation and Entrepreneurship Training Program in 2021(No.202110163003).
文摘Epicatechin gallate(ECG)is one of the polyphenolic compounds and has attracted much attention due to its various bioactivities.In this study,the neuroprotective eff ect of ECG against H_(2)O_(2)-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 H_(2)O_(2)-induced oxidative injury by using the RNA-seq method.Finally,the change in the cell cycle was analyzed by fl ow cytometry.H_(2)O_(2)(400-1200μmol/L)inhibited the cell viability in a concentration-dependent manner.ECG(6-150μmol/L)eff ectively attenuated the H_(2)O_(2)-induced decrease in cell viability.RNA-seq analysis showed that ECG regulated 1058 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 H_(2)O_(2)-induced oxidative injury and 28 coexpressed DEGs in the cell cycle pathway were summarized.Finally,cell cycle analysis also proved that ECG improved H_(2)O_(2)-induced cell cycle arrest in the G2/M phase.Our present study demonstrated that ECG attenuated H_(2)O_(2)-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.
