Research Article | | Peer-Reviewed

Chlorogenic Acid Inhibition HBV Replication by Suppressed JNK Expression

Received: 6 August 2024     Accepted: 28 August 2024     Published: 20 September 2024
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Abstract

Aim: Hepatitis B virus is a primary etiological factor for various liver diseases, including cirrhosis and hepatocellular carcinoma.Hepatitis B virus is an incomplete double-stranded DNA virus, which infects hepatic cells, enters the nucleus to form a complete double-stranded DNA and products a series of functional proteins, then replicates and assembles to form a complete virus, which is released outside the cell. So far, the pathogenesis of hepatitis B virus is not clear. JNK signaling pathway is an important branch of MAPK pathway, which plays an important role in various physiological and pathological processes such as cell cycle, reproduction, apoptosis and cell stress. Study show JNK activation involves liver damage. Especially, hepatitis B virus infection promote the phosphorylation of JNK. Chlorogenic acid, as a polyphenolic compound, exhibits notable antioxidant and antiviral properties. Study revealed chlorogenic acid had ability of inhibiting hepatitis B virus replication, but the mechanisms was unknown. Here we demonstrated the antiviral mechanisms of chlorogenic acd on HBV replication. Methods: To investigate the effect of chlorogenic acid on HBV replication, southern blot and western blot were performed using HepAD38 cells. Results: Chlorogenic acid suppressed HBV replication. In this process, JNK expression was inhibited. Conclusion: chlorogenic acid suppressed HBV replication via inhibiting JNK expression.

Published in Clinical Medicine Research (Volume 13, Issue 5)
DOI 10.11648/j.cmr.20241305.11
Page(s) 55-59
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Chlorogenic Acid, HBV, JNK

References
[1] Xiao, Y., et al., Discrepant results of hepatitis B virus genotype determination by PCR and DNA sequencing. Journal of Virological Methods, 2022. 303: p. 114503.
[2] Korkmaz, P., et al., New Treatment Options in Chronic Hepatitis B: How Close Are We to Cure? Infectious Diseases & Clinical Microbiology, 2023. 5(4): p. 267.
[3] Acharya, C., & Bajaj, J. S.Chronic Liver Diseases and the Microbiome-Translating Our Knowledge of Gut Microbiota to Management of Chronic Liver Disease. Gastroenterology, 2021, 160(2), 556–572.
[4] Zhang, M., et al., Persistent steatosis correlates with decreased fibrosis regression during anti-HBV treatment in patients with chronic HBV infection. Journal of medical virology, 2023, 95(10), e29156.
[5] Jose-Abrego, A., et al., Host and HBV Interactions and Their Potential Impact on Clinical Outcomes.Pathogens, 2023, 12(9), 1146.
[6] Huang, J., et al., Chlorogenic acid: a review on its mechanisms of anti-inflammation, disease treatment, and related delivery systems.Frontiers in pharmacology, 2023, 14, 1218015.
[7] Shi, H., et al., Chlorogenic acid protects against liver fibrosis in vivo and in vitro through inhibition of oxidative stress. Clinical Nutrition, 2016. 35(6): p. 1366-1373.
[8] Wang, G.-F., et al., Anti-hepatitis B virus activity of chlorogenic acid, quinic acid and caffeic acid in vivo and in vitro. Antiviral Research, 2009. 83(2): p. 186-190.
[9] Chatzifrangkeskou, M., et al., JNK regulates ciliogenesis through the interflagellar transport complex and actin networks. The Journal of cell biology, 2023, 222(11), e202303052.
[10] Li, X., et al., JNK/c-Jun pathway activation is essential for HBx-induced IL-35 elevation to promote persistent HBV infection. Journal of Clinical Laboratory Analysis, 2023. 37(5).
[11] Wang, L., et al., Orexin A ameliorates HBV X protein-induced cytotoxicity and inflammatory response in human hepatocytes. Artificial Cells, Nanomedicine, and Biotechnology, 2019. 47(1): p. 2003-2009.
[12] Zhong, L., et al., Reactive Oxygen Species-Mediated c-Jun NH2-Terminal Kinase Activation Contributes to Hepatitis B Virus X Protein-Induced Autophagy via Regulation of the Beclin-1/Bcl-2 Interaction. Journal of Virology, 2017. 91(15).
[13] Zhang, C., et al., C-terminal-truncated hepatitis B virus X protein promotes hepatocarcinogenesis by activating the MAPK pathway. Microbial Pathogenesis, 2021. 159: p. 105136.
[14] Wang, F., et al., Role of hepatitis B virus non-structural protein HBx on HBV replication, interferon signaling, and hepatocarcinogenesis. Frontiers in microbiology, 2023, 14, 1322892.
[15] Yin, M., et al., Exosomes from hepatitis B virus-infected hepatocytes activate hepatic stellate cells and aggravate liver fibrosis through the miR-506-3p/Nur77 pathway. Journal of biochemical and molecular toxicology, 2023, 37(10), e23432.
Cite This Article
  • APA Style

    Lai, L., Li, L., Cui, X., Piao, L., Cui, Z. (2024). Chlorogenic Acid Inhibition HBV Replication by Suppressed JNK Expression. Clinical Medicine Research, 13(5), 55-59. https://doi.org/10.11648/j.cmr.20241305.11

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    ACS Style

    Lai, L.; Li, L.; Cui, X.; Piao, L.; Cui, Z. Chlorogenic Acid Inhibition HBV Replication by Suppressed JNK Expression. Clin. Med. Res. 2024, 13(5), 55-59. doi: 10.11648/j.cmr.20241305.11

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    AMA Style

    Lai L, Li L, Cui X, Piao L, Cui Z. Chlorogenic Acid Inhibition HBV Replication by Suppressed JNK Expression. Clin Med Res. 2024;13(5):55-59. doi: 10.11648/j.cmr.20241305.11

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  • @article{10.11648/j.cmr.20241305.11,
      author = {Lan Lai and Lihua Li and Xiuji Cui and Linghua Piao and Zhigang Cui},
      title = {Chlorogenic Acid Inhibition HBV Replication by Suppressed JNK Expression
    },
      journal = {Clinical Medicine Research},
      volume = {13},
      number = {5},
      pages = {55-59},
      doi = {10.11648/j.cmr.20241305.11},
      url = {https://doi.org/10.11648/j.cmr.20241305.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cmr.20241305.11},
      abstract = {Aim: Hepatitis B virus is a primary etiological factor for various liver diseases, including cirrhosis and hepatocellular carcinoma.Hepatitis B virus is an incomplete double-stranded DNA virus, which infects hepatic cells, enters the nucleus to form a complete double-stranded DNA and products a series of functional proteins, then replicates and assembles to form a complete virus, which is released outside the cell. So far, the pathogenesis of hepatitis B virus is not clear. JNK signaling pathway is an important branch of MAPK pathway, which plays an important role in various physiological and pathological processes such as cell cycle, reproduction, apoptosis and cell stress. Study show JNK activation involves liver damage. Especially, hepatitis B virus infection promote the phosphorylation of JNK. Chlorogenic acid, as a polyphenolic compound, exhibits notable antioxidant and antiviral properties. Study revealed chlorogenic acid had ability of inhibiting hepatitis B virus replication, but the mechanisms was unknown. Here we demonstrated the antiviral mechanisms of chlorogenic acd on HBV replication. Methods: To investigate the effect of chlorogenic acid on HBV replication, southern blot and western blot were performed using HepAD38 cells. Results: Chlorogenic acid suppressed HBV replication. In this process, JNK expression was inhibited. Conclusion: chlorogenic acid suppressed HBV replication via inhibiting JNK expression.
    },
     year = {2024}
    }
    

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  • TY  - JOUR
    T1  - Chlorogenic Acid Inhibition HBV Replication by Suppressed JNK Expression
    
    AU  - Lan Lai
    AU  - Lihua Li
    AU  - Xiuji Cui
    AU  - Linghua Piao
    AU  - Zhigang Cui
    Y1  - 2024/09/20
    PY  - 2024
    N1  - https://doi.org/10.11648/j.cmr.20241305.11
    DO  - 10.11648/j.cmr.20241305.11
    T2  - Clinical Medicine Research
    JF  - Clinical Medicine Research
    JO  - Clinical Medicine Research
    SP  - 55
    EP  - 59
    PB  - Science Publishing Group
    SN  - 2326-9057
    UR  - https://doi.org/10.11648/j.cmr.20241305.11
    AB  - Aim: Hepatitis B virus is a primary etiological factor for various liver diseases, including cirrhosis and hepatocellular carcinoma.Hepatitis B virus is an incomplete double-stranded DNA virus, which infects hepatic cells, enters the nucleus to form a complete double-stranded DNA and products a series of functional proteins, then replicates and assembles to form a complete virus, which is released outside the cell. So far, the pathogenesis of hepatitis B virus is not clear. JNK signaling pathway is an important branch of MAPK pathway, which plays an important role in various physiological and pathological processes such as cell cycle, reproduction, apoptosis and cell stress. Study show JNK activation involves liver damage. Especially, hepatitis B virus infection promote the phosphorylation of JNK. Chlorogenic acid, as a polyphenolic compound, exhibits notable antioxidant and antiviral properties. Study revealed chlorogenic acid had ability of inhibiting hepatitis B virus replication, but the mechanisms was unknown. Here we demonstrated the antiviral mechanisms of chlorogenic acd on HBV replication. Methods: To investigate the effect of chlorogenic acid on HBV replication, southern blot and western blot were performed using HepAD38 cells. Results: Chlorogenic acid suppressed HBV replication. In this process, JNK expression was inhibited. Conclusion: chlorogenic acid suppressed HBV replication via inhibiting JNK expression.
    
    VL  - 13
    IS  - 5
    ER  - 

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Author Information
  • Key Laboratory of Tropic Translational Medicine of Ministry of Education, School of Basic Medicine and Life Sciences, Hainan Medical University, Haikou City, China

  • Key Laboratory of Tropic Translational Medicine of Ministry of Education, School of Basic Medicine and Life Sciences, Hainan Medical University, Haikou City, China

  • Key Laboratory of Tropic Translational Medicine of Ministry of Education, School of Basic Medicine and Life Sciences, Hainan Medical University, Haikou City, China

  • Key Laboratory of Tropic Translational Medicine of Ministry of Education, School of Basic Medicine and Life Sciences, Hainan Medical University, Haikou City, China

  • Key Laboratory of Tropic Translational Medicine of Ministry of Education, School of Basic Medicine and Life Sciences, Hainan Medical University, Haikou City, China

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