{"title":"Notoginsenoside R1 inhibits hepatitis B virus replication by modulating SIRT1 activity.","authors":"Wujing Zhang, Jingjing Cui, Lichun Li, Lijuan Chai, Qingling Hou, Huaqi Yu","doi":"10.4149/av_2023_105","DOIUrl":null,"url":null,"abstract":"<p><p>The hepatitis B virus (HBV) infection remains highly prevalent globally. The present study aimed to explore the possible therapeutic effect of notoginsenoside R1, which has attracted considerable attention due to its diverse pharmacological effects, on HBV infection. The HBV-containing hepatocellular carcinoma cell lines, HepG2 and MHCC97H, were used in this study. We first treated the two cell lines with different concentrations of notoginsenoside R1 and subsequently measured the relative levels of HBV DNA, HBV surface antigen, HBV core antigen, and sirtuin 1 (SIRT1) using reverse transcription-quantitative polymerase chain reaction and western blotting. Finally, an HBV hemodynamic replication model was created to test the effect of notoginsenoside R1 on HBV replication. Notoginsenoside R1 inhibited the replication of HBV. This inhibitory effect was mediated through the downregulation of SIRT1 activity. Additionally, the inhibition of SIRT1 activity by silencing its expression or treatment with the SIRT1 inhibitor, selisistat, suppressed HBV replication. Furthermore, our animal experiments demonstrated that notoginsenoside R1 was effective at suppressing HBV replication in vivo. Thus, notoginsenoside R1 suppresses HBV replication by downregulating SIRT1 activity in vitro and in vivo. Keywords: notoginsenoside R1; hepatitis B virus; SIRT1.</p>","PeriodicalId":7205,"journal":{"name":"Acta virologica","volume":"67 1","pages":"51-58"},"PeriodicalIF":1.1000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta virologica","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.4149/av_2023_105","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"VIROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
The hepatitis B virus (HBV) infection remains highly prevalent globally. The present study aimed to explore the possible therapeutic effect of notoginsenoside R1, which has attracted considerable attention due to its diverse pharmacological effects, on HBV infection. The HBV-containing hepatocellular carcinoma cell lines, HepG2 and MHCC97H, were used in this study. We first treated the two cell lines with different concentrations of notoginsenoside R1 and subsequently measured the relative levels of HBV DNA, HBV surface antigen, HBV core antigen, and sirtuin 1 (SIRT1) using reverse transcription-quantitative polymerase chain reaction and western blotting. Finally, an HBV hemodynamic replication model was created to test the effect of notoginsenoside R1 on HBV replication. Notoginsenoside R1 inhibited the replication of HBV. This inhibitory effect was mediated through the downregulation of SIRT1 activity. Additionally, the inhibition of SIRT1 activity by silencing its expression or treatment with the SIRT1 inhibitor, selisistat, suppressed HBV replication. Furthermore, our animal experiments demonstrated that notoginsenoside R1 was effective at suppressing HBV replication in vivo. Thus, notoginsenoside R1 suppresses HBV replication by downregulating SIRT1 activity in vitro and in vivo. Keywords: notoginsenoside R1; hepatitis B virus; SIRT1.
期刊介绍:
Acta virologica is an international journal of predominantly molecular and cellular virology. Acta virologica aims to publish papers reporting original results of fundamental and applied research mainly on human, animal and plant viruses at cellular and molecular level. As a matter of tradition, also rickettsiae are included. Areas of interest are virus structure and morphology, molecular biology of virus-cell interactions, molecular genetics of viruses, pathogenesis of viral diseases, viral immunology, vaccines, antiviral drugs and viral diagnostics.