Effectiveness of Low Molecular Weight Fucoidan and High Stability Fucoxanthin (LMF- HSFX) in Phaeophyta as Bioactivity in Emergency Therapy of Non-Alcoholic Fatty Liver Disease (NAFLD)

Authors

  • Norina Agatri Universitas Muhammadiyah Purwokerto
  • Nimas Adiani Sekar Laranti Universitas Muhammadiyah Purwokerto
  • Hanifa Nur Shabrina Universitas Muhammadiyah Purwokerto
  • Fatmanur Hurulhanifa Universitas Muhammadiyah Purwokerto

DOI:

https://doi.org/10.30595/hmj.v7i1.23150

Keywords:

Phaeophyta, Low Molecular Weight Fucoidan, High Stability Fucoxanthin, Non-Alcoholic Fatty Liver Disease, Bioactivity, Biocompatibility, Hepatic lipotoxicity

Abstract

Indonesia is a maritime nation with a rich marine ecosystem and biodiversity. The waters are abundant in Phaeophyta (brown algae), which are a significant source of bioactive compounds such as fucoidan and fucoxanthin. These compounds have shown potential in treating Non-Alcoholic Fatty Liver Disease (NAFLD), a metabolic disorder characterized by excessive fat accumulation in the liver, leading to complications such as fibrosis, cirrhosis, and hepatocellular carcinoma. The objective of this study is to evaluate the effectiveness of Low Molecular Weight Fucoidan (LMF) and High Stability Fucoxanthin (HSFx) in the curative treatment of NAFLD. Specifically, the study aims to assess the bioactivity and biocompatibility of LMF-HSFx and compare its efficacy with a placebo group in the treatment of NAFLD. The study used a non-invasive Fibroscan to test Controlled Attenuation Parameter (CAP) and Transient Elastography on NAFLD patients. It included 42 NAFLD patients, divided into two groups: the LMF-HSFx group and the placebo group. The LMF-HSFx group received oral supplementation of 825 mg LMF fucoidan and 825 mg HSFx twice daily for six months. The effectiveness of the treatment was measured through changes in hepatic lipotoxicity, serum markers, and pro-inflammatory cytokines. The results showed significant reductions in hepatic lipotoxicity, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol, and triglycerides in the LMF-HSFx group. The study also observed significant reductions in pro-inflammatory cytokines (IL-6 and IFN-γ) and improvements in adiponectin and leptin levels. These findings suggest that the LMF-HSFx combination effectively reduces hepatic inflammation and improves metabolic parameters in NAFLD patients.

References

1. Litaay C. DISTRIBUTIONAND DIVERSITY OF MACRO ALGAE COMMUNITIES

IN THE AMBON BAY [Internet]. Vol. 6, Journal of Tropical Marine Science and Technology. Available from: http://itk.fpik.ipb.ac.id/ej_itkt61

2. Aulia A. Morphological identification of some species of Phaeophyta members at Cibeureum Palm Beach, Anyer, Banten. 2021;1.

3. Shih PH, Shiue SJ, Chen CN, Cheng SW, Lin HY, Wu LW, et al. Fucoidan and Fucoxanthin Attenuate Hepatic Steatosis and Inflammation of NAFLD through Modulation of Leptin/Adiponectin Axis. Mar Drugs. 2021 Mar 12;19(3):148.

4. El Rashed ZeinabGElenaKH. Brown-Algae Polysaccharides as Active Constituents against Nonalcoholic Fatty Liver Disease. 2020;

5. Hidayati JR, Bahry MS, Karlina I, Yudiati E. Antioxidant Activity and Bioactive Compounds of Tropical Brown Algae Padina sp. from Bintan Island, Indonesia. Journal of Tropical Marine. 2022 Nov 1;25(3):309-19.

6. Younossi ZM, Wong G, Anstee QM, Henry L. The Global Burden of Liver Disease. Clinical Gastroenterology and Hepatology. Jul 2023;21(8):1978-91.

7. Cheemerla DBM. Global Epidemiology of Chronic Liver Disease. PubMed. 2021;17:365-70.

8. Collaborators GBDC. The global, regional, and national burden of cirrhosis by cause in 195 countries and territories, 1990-2017: A systematic analysis for the Global Burden of Disease Study 2017. Lancet Gastroenterol. 2020;5:245-66.

9. Kazankov K JSTKMH. The role of macrophages in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. . Nat Rev Gastroenterol. 2019;16:145-59.

10. Mantovani A, Dalbeni A. Treatments for nafld: State of art. Vol. 22, International Journal of Molecular Sciences. MDPI AG; 2021. p. 1-27.

11. Wayan Rosiana I, Angga Wiradana P, Gede Widhiantara I, Agung Ayu Putri Permatasari A, Kadek Yunita Sari N, Made Gde Sudyadnyana Sandhika I, et al. An Overview of Brown Macroalgae Extract Against Fatty Liver Disease Caused by Metabolic Dysfunction: Animal Models and Evidence in Human Trials. Vol. 2023, Chem. Bull.

12. Lourenco-Lopes C; FCM; JLC; CM; PA; GOP, Prieto M; SGJ. Biological action mechanism of fucoxanthin extracted from algae for application in food and cosmetic industries. Trends Food Sci. 2021;(117):163-81.

13. Murase W; KY; KS; YA; WM; KA, Kojima H; OT; TM; MM; et al. Fucochanthin Prevents Pancreatic Tumorigenesis in C57BL/6J Mice That Received Allogenic and Orthotopic Transplants of Cancer Cells. PubMed. 2021;22:13620.

14. Terasaki M; KA; KH; MH; MK; KC;, Mutoh M; TT. Fucoxanthin and Colorectal Cancer Prevention. CrossRef. 2021;13:2379.

15. Suprunchuk VE. Low-molecular-weight fucoidan: Chemical modification, synthesis of its oligomeric fragments and mimetics. Carbohydr Res. 2019 Nov;485:107806.

16. Din NAS, Mohd Alayudin 'Ain Sajda, Sofian-Seng NS, Rahman HA, Mohd Razali NS, Lim SJ, et al. Brown Algae as Functional Food Source of Fucoxanthin: A Review. Vol. 11, Foods. MDPI; 2022.

17. Luthuli S; WS; CY; ZX; WM; TH. Therapeutic Effects of Fucoidan: A Review on Recent Studies. CrossRef. 2019;17:487.

18. Citkowska A, Szekalska M, Winnicka K. Possibilities of Fucoidan Utilization in the Development of Pharmaceutical Dosage Forms. Mar Drugs. 2019 Aug 5;17(8):458.

19. Winarto J, Song DG, Pan CH. The Role of Fucoxanthin in Non-Alcoholic Fatty Liver Disease. Int J Mol Sci. May 2023;24(9):8203.

20. Ren T, Zhu L, Shen Y, Mou Q, Lin T, Feng H. Protection of hepatocyte mitochondrial function by blueberry juice and probiotics via SIRT1 regulation in non-alcoholic fatty liver disease. CrossRef. 2019;10:1540-51.

21. Raffaele M, Bellner L, Singh SP, Favero G, Rezzani R, Rodella LF, et al. Epoxyeicoisatrienoic intervention improves NAFLD in leptin receptor deficient mice by an increase in PGC1α-HO-1-PGC1α- mitochondrial signaling. PubMed. 2019;(380):180-7.

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Published

2024-04-30