Razieh Dowran - Department of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
Seyed Younes Hosseini - Department of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Mohammad Reza Fattahi - Gastroenterohepatology Research center, Shiraz University of Medical Sciences, Shiraz, Iran
Jamal Sarvari - Department of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.Gastroenterohepatology Research center, Shiraz University of Medical Sciences, Shiraz, Iran

Introduction: Silibinin (silibinin A) is the most active silymarin component, which acts both as a hepatoprotective [۱] and an antiviral agent. The present study investigated the silibinin effect on IFN-related innate immune genes in PBMCs from HCV-infected patients. Method: ۲۲ chronic HCV patients, including ۱۰ IFN responders and ۱۲ non-responders, were included. Their isolated PBMCs were treated for ۶ hours in the presence of silibinin, IFN-α, or their combination. The transcription level of TLR۷, ISG۱۵, and SOCS۱ genes was compared using real-time PCR. Result: Our result showed that IFN-α induced a significant up-regulation of TLR۷ and ISG۱۵ in PBMCs of both responder and non-responder groups. Nevertheless, the SOCS۱ gene was not significantly changed in the non-responder group (P=۰.۳۲). 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 TLR۷, ISG۱۵, and SOCS۱ genes.  Therefore, it has been suggested that its anti-inflammatory role might be devoid of IFN pathways.

HCV, Silibinin, Interferon, ISG۱۵, SOCS۱