Allicin inhibits HBV replication through the HBV promoter SP2

Objective To investigate the effect of allicin on the replication of hepatitis B virus (HBV) and to preliminarily elucidate its underlying molecular mechanisms. Methods HepG 2.2.15 cells were treated with different concentrations of allicin and the levels of HBsAg and HBeAg were assessed by ELISA....

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Main Author: LU Lili, ZHU Xilin, WU Xiaopan, LIU Ying
Format: Article
Language:zho
Published: Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College. 2025-04-01
Series:Jichu yixue yu linchuang
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Online Access:https://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/1001-6325-2025-45-4-465.pdf
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author LU Lili, ZHU Xilin, WU Xiaopan, LIU Ying
author_facet LU Lili, ZHU Xilin, WU Xiaopan, LIU Ying
author_sort LU Lili, ZHU Xilin, WU Xiaopan, LIU Ying
collection DOAJ
description Objective To investigate the effect of allicin on the replication of hepatitis B virus (HBV) and to preliminarily elucidate its underlying molecular mechanisms. Methods HepG 2.2.15 cells were treated with different concentrations of allicin and the levels of HBsAg and HBeAg were assessed by ELISA. Cell viability was evaluated using the CCK-8 assay to determine the optimal concentration of allicin; HepG2-NTCP cells were incubated with the optimal concentration of allicin for 48 hours, and the expression of HBV-related markers was detected by RT-qPCR; The activity of four HBV promoters (Enh Ⅰ/Xp, SP1, SP2, and CP) was analyzed using a dual-luciferase reporter gene experiment. The effect of allicin on promoter activity was assessed; Gene-regulation tools were used to predict potential transcription factor that might bind to the promoter. After over-expressing the transcription factor, cells were incubated with allicin and the effect on promoter activity was examined; Finally, ChIP was used to confirm whether these transcription factors bind to the HBV promoters and whether allicin treatment affects this binding. Results Allicin significantly reduced the expression of HBsAg and slightly lowered the expression of HBeAg(P<0.001); A concentration of 40 μmol/L allicin significantly inhibited HBV DNA replication and transcription(P<0.05), without affecting cell viability; Allicin also significantly suppressed the activity of the HBV promoter SP2(P<0.001). Further investigation revealed that the transcription factor SP1 could bind to the DNA sequence of the HBV promoter SP2, and this binding was significantly inhibited after allicin treatment(P<0.001). Conclusions Allicin inhibits the binding of the transcription factor SP1 to HBV promoter SP2, thereby reducing the transcriptional activity of HBV and suppressing viral replication.
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spelling doaj-art-df0723ebf2564b85966749a30b0bb40a2025-08-20T02:53:57ZzhoInstitute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College.Jichu yixue yu linchuang1001-63252025-04-0145446547010.16352/j.issn.1001-6325.2025.04.0465Allicin inhibits HBV replication through the HBV promoter SP2LU Lili, ZHU Xilin, WU Xiaopan, LIU Ying0Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences CAMS, School of Basic Medicine PUMC, Beijing 100005, ChinaObjective To investigate the effect of allicin on the replication of hepatitis B virus (HBV) and to preliminarily elucidate its underlying molecular mechanisms. Methods HepG 2.2.15 cells were treated with different concentrations of allicin and the levels of HBsAg and HBeAg were assessed by ELISA. Cell viability was evaluated using the CCK-8 assay to determine the optimal concentration of allicin; HepG2-NTCP cells were incubated with the optimal concentration of allicin for 48 hours, and the expression of HBV-related markers was detected by RT-qPCR; The activity of four HBV promoters (Enh Ⅰ/Xp, SP1, SP2, and CP) was analyzed using a dual-luciferase reporter gene experiment. The effect of allicin on promoter activity was assessed; Gene-regulation tools were used to predict potential transcription factor that might bind to the promoter. After over-expressing the transcription factor, cells were incubated with allicin and the effect on promoter activity was examined; Finally, ChIP was used to confirm whether these transcription factors bind to the HBV promoters and whether allicin treatment affects this binding. Results Allicin significantly reduced the expression of HBsAg and slightly lowered the expression of HBeAg(P<0.001); A concentration of 40 μmol/L allicin significantly inhibited HBV DNA replication and transcription(P<0.05), without affecting cell viability; Allicin also significantly suppressed the activity of the HBV promoter SP2(P<0.001). Further investigation revealed that the transcription factor SP1 could bind to the DNA sequence of the HBV promoter SP2, and this binding was significantly inhibited after allicin treatment(P<0.001). Conclusions Allicin inhibits the binding of the transcription factor SP1 to HBV promoter SP2, thereby reducing the transcriptional activity of HBV and suppressing viral replication.https://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/1001-6325-2025-45-4-465.pdfallicin|hepatitis b virus|antiviral|transcriptional regulation|hbv promoter sp2
spellingShingle LU Lili, ZHU Xilin, WU Xiaopan, LIU Ying
Allicin inhibits HBV replication through the HBV promoter SP2
Jichu yixue yu linchuang
allicin|hepatitis b virus|antiviral|transcriptional regulation|hbv promoter sp2
title Allicin inhibits HBV replication through the HBV promoter SP2
title_full Allicin inhibits HBV replication through the HBV promoter SP2
title_fullStr Allicin inhibits HBV replication through the HBV promoter SP2
title_full_unstemmed Allicin inhibits HBV replication through the HBV promoter SP2
title_short Allicin inhibits HBV replication through the HBV promoter SP2
title_sort allicin inhibits hbv replication through the hbv promoter sp2
topic allicin|hepatitis b virus|antiviral|transcriptional regulation|hbv promoter sp2
url https://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/1001-6325-2025-45-4-465.pdf
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