Journal of Convergence Korean Medicine (대한융합한의학회지)

Academy of Convergence Korean Medicine (대한융합한의학회)
권호 표지

Protective effects against alcoholic liver damage: potential of herbal juice (HJ), blend of Zingiber officinale Roscoe and Pueraria lobata Ohwi extracts

  • Young Yun Jung (Department of Science in Korean Medicine, Kyung Hee University) ;
  • You Yeon Choi (Department of Convergence Korean Medical Science, Kyung Hee University) ;
  • Woong Mo Yang (Department of Convergence Korean Medical Science, Kyung Hee University) ;
  • Kwang Seok Ahn (Department of Science in Korean Medicine, Kyung Hee University)
  • Received : 2023.05.04
  • Accepted : 2023.06.28
  • Published : 2023.06.30
Download PDF
⟨ Previous Next ⟩

Abstract

Objectives : Alcohol-induced liver disease advances as to reactive oxygen species (ROS) and cellular lipid peroxidation increase. We examined the hepatoprotective effects of Zingiber officinale Roscoe rhizome extract (ZR), Pueraria lobata Ohwi flower extracts (PF), and a newly developed herbal juice (HJ), which was a combination of ZR and PF extracts, against ethanol-induced hepatotoxicity. Methods: The study utilized the human hepatoma cell line HepG2 cells to validate the hepatoprotective effect of HJ (50~200 ㎍/mL) against ethanol (EtOH, 700 mM)-induced liver damage. Results: HJ effectively reduced the protein expression of sterol regulatory element-binding transcription factor 1, adiponectin, and AMP-activated protein kinase in EtOH-induced HepG2 cells. The levels of ROS, total cholesterol, and triglycerides, which are the result of various synthesis and lipogenesis processes induced by EtOH in the liver, were reduced by HJ. Furthermore, the activities of alcohol dehydrogenase and aldehyde dehydrogenase, enzymes linked to alcohol degradation, were more effectively downregulated by HJ treatment compared to treatment with ZR and PF alone, all without causing cytotoxic effects. Conclusions: HJ protects the liver by inhibiting EtOH-induced lipogenesis, lowering ROS generation, and improving alcohol degradation, which is more effective than ZR and PF alone. Further, in vivo experiments can offer additional evidence regarding the effectiveness, safety, and underlying mechanism of action of HJ.

Keywords

References

  1. Kalra A, Yetiskul E, Wehrle CJ, Tuma F. Physiology, Liver. Treasure Island (FL) ineligible companies. StatPearls Publishing; Jan 2023. 
  2. Han YH, He XM, Jin MH, Sun HN, Kwon T. Lipophagy: A potential therapeutic target for nonalcoholic and alcoholic fatty liver disease. Biochem Biophys Res Commun. 2023;672:36-44.  https://doi.org/10.1016/j.bbrc.2023.06.030
  3. Xu F, Mandarino N, Zoccali P, Bonanno A. Al atomic Auger electron emission from low-keV-ion-bombarded Al surfaces. Phys Rev A. 1992;46:2613-7.  https://doi.org/10.1103/PhysRevA.46.2613
  4. You M, Fischer M, Deeg MA, Crabb DW. Ethanol induces fatty acid synthesis pathways by activation of sterol regulatory element-binding protein (SREBP). J Biol Chem. 2002;277:29342-29347.  https://doi.org/10.1074/jbc.M202411200
  5. Brown MS, Goldstein JL. A proteolytic pathway that controls the cholesterol content of membranes, cells, and blood. Proc Natl Acad Sci U S A. 1999;96:11041-8.  https://doi.org/10.1073/pnas.96.20.11041
  6. Shimano H, Horton JD, Hammer RE, Shimomura I, Brown MS, Goldstein JL. Overproduction of cholesterol and fatty acids causes massive liver enlargement in transgenic mice expressing truncated SREBP-1a. J Clin Invest. 1996;98:1575-1584.  https://doi.org/10.1172/JCI118951
  7. Horton JD, Shimomura I, Brown MS, Hammer RE, Goldstein JL, Shimano H. Activation of cholesterol synthesis in preference to fatty acid synthesis in liver and adipose tissue of transgenic mice overproducing sterol regulatory element-binding protein-2. J Clin Invest. 1998;101:2331-9.  https://doi.org/10.1172/JCI2961
  8. Awazawa M, Ueki K, Inabe K, et al. Adiponectin suppresses hepatic SREBP1c expression in an AdipoR1/LKB1/AMPK dependent pathway. Biochem Biophys Res Commun. 2009;382:51-6.  https://doi.org/10.1016/j.bbrc.2009.02.131
  9. Bailey SM, Cunningham CC. Acute and chronic ethanol increases reactive oxygen species generation and decreases viability in fresh, isolated rat hepatocytes. Hepatology. 1998;28:1318-1326.  https://doi.org/10.1002/hep.510280521
  10. Tan HK, Yates E, Lilly K, Dhanda AD. Oxidative stress in alcohol-related liver disease. World J Hepatol. 2020;12:332-349.  https://doi.org/10.4254/wjh.v12.i7.332
  11. Crabb DW, Matsumoto M, Chang D, You M. Overview of the role of alcohol dehydrogenase and aldehyde dehydrogenase and their variants in the genesis of alcohol-related pathology. Proc Nutr Soc. 2004;63:49-63.  https://doi.org/10.1079/PNS2003327
  12. Jelski W, Szmitkowski M. Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) in the cancer diseases. Clin Chim Acta. 2008;395:1-5.  https://doi.org/10.1016/j.cca.2008.05.001
  13. Mahbub AA, Le Maitre CL, Haywood-Small SL, Cross NA, Jordan-Mahy N. Polyphenols act synergistically with doxorubicin and etoposide in leukaemia cell lines. Cell Death Discov. 2015;1:15043. 
  14. Dai X, Wang L, Deivasigamni A, et al. A novel benzimidazole derivative, MBIC inhibits tumor growth and promotes apoptosis via activation of ROS-dependent JNK signaling pathway in hepatocellular carcinoma. Oncotarget. 2017;8:12831-12842. https://doi.org/10.18632/oncotarget.14606