The Effect of Silibinin on the Expression of TLR7, ISG15, and SOCS1 in Peripheral Blood Mononuclear Cells of Hepatitis C Infected Patients in Comparison with Interferon-α
{"title":"The Effect of Silibinin on the Expression of TLR7, ISG15, and SOCS1 in Peripheral Blood Mononuclear Cells of Hepatitis C Infected Patients in Comparison with Interferon-α","authors":"R. Dowran, S. Hosseini, M. Fattahi, J. Sarvari","doi":"10.52547/JOMMID.9.1.12","DOIUrl":null,"url":null,"abstract":"Background: Silibinin (silibinin A) is the most active silymarin component, which acts both as a hepatoprotective [1] and an antiviral agent. The present study investigated the silibinin effect on IFN-related innate immune genes in PBMCs from HCV-infected patients. Method: 22 chronic HCV patients, including 10 IFN responders and 12 non-responders, were included. Their isolated PBMCs were treated for 6 hours in the presence of silibinin, IFN-α, or their combination. The transcription level of TLR7, ISG15, and SOCS1 genes was compared using real-time PCR. Result: Our result showed that IFN-α induced a significant up-regulation of TLR7 and ISG15 in PBMCs of both responder and non-responder groups. Nevertheless, the SOCS1 gene was not significantly changed in the non-responder group (P=0.32). The combination of IFNα- and silibinin showed a similar pattern to IFN-α alone. By itself, silibinin did not leave a significant change on the expression level of the studied genes . Conclusion: The results indicated that silibinin did not enhance or suppress the expression level of TLR7, ISG15, and SOCS1 genes. Therefore, it has been suggested that its anti-inflammatory role might be devoid of IFN pathways.","PeriodicalId":34460,"journal":{"name":"Journal of Medical Microbiology and Infectious Diseases","volume":"84 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Medical Microbiology and Infectious Diseases","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.52547/JOMMID.9.1.12","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Silibinin (silibinin A) is the most active silymarin component, which acts both as a hepatoprotective [1] and an antiviral agent. The present study investigated the silibinin effect on IFN-related innate immune genes in PBMCs from HCV-infected patients. Method: 22 chronic HCV patients, including 10 IFN responders and 12 non-responders, were included. Their isolated PBMCs were treated for 6 hours in the presence of silibinin, IFN-α, or their combination. The transcription level of TLR7, ISG15, and SOCS1 genes was compared using real-time PCR. Result: Our result showed that IFN-α induced a significant up-regulation of TLR7 and ISG15 in PBMCs of both responder and non-responder groups. Nevertheless, the SOCS1 gene was not significantly changed in the non-responder group (P=0.32). The combination of IFNα- and silibinin showed a similar pattern to IFN-α alone. By itself, silibinin did not leave a significant change on the expression level of the studied genes . Conclusion: The results indicated that silibinin did not enhance or suppress the expression level of TLR7, ISG15, and SOCS1 genes. Therefore, it has been suggested that its anti-inflammatory role might be devoid of IFN pathways.